Can you get discriminated for an anxiety/depression disorder that has been treat!
Question: I applied for a postion working for the government. I passed the drug and physcial exam except for the medicines that I am taking. I received a phone call from the company because they want more information about the medicines that I take for anxiety (for panic attacks which then resulted in depression because I had no idea what that was and was in denial about it). I passed the physical exam but the doctor won't sign the paper until I talk to a counselor. If I was diagnosed in 2004, which is two years ago, can they
rescind the job offer? I have been stabalized on medication so I do not know why it is an issue. It is a huge corporation but it is private. The nurse will not be in for the phone "evaluation" tomorrow but will call me on Monday. Should I be worried? This phone call created more anxiety!
Thank you for your help!
Answers:
I sincerely don't think they can rescind the job offer based on a mental health illness that you are being treated for. If this were the case,most of the population would be unemployed!
Your personal medical files are private,because of the HIPA laws. You actually don't have to give them any information.
Other Answers:
yes
Try to relax about it sweetheart.People are afraid of what they do not understand. You will be discriminated against for the rest of your life for this disorder that you have no control over. You have to know that this is not your fault or your problem. Take care and be strong. :^)
It depends on the job. If they ask you if you can handle a high pressure position. maybe because the meds and anxiety prove no. But legally they could get in trouble for denying you a job just because you take meds.
Source(s):
I have a teen on anti-anxiety meds and am a SPED teacher, Sped law, etc.
they shouldn't be able to discriminate since you're taking appropriate steps to manage the condition. unfortunately, they can do whatever they want. they'll probably give some other lame bogus reason if they don't hire you and you won't be able to prove what the real reason is even though it seems obvious. good luck.
This exactly depends on the job you've applied to.You have done the best think you an do by telling them the truth.All you can do is to wait and see now.
Is it the drug testing company that's calling or your potential employer? Either way, don't panic. It's likely that something showed up in your whiz quiz and they want clarification to ensure that you're taking legitimately prescribed drugs.
A little more info that may or may not be pertinent:
If you are applying for a job in which your company may be contracting you out for a government position which requires a security clearance, they may rescind the job offer if it appears that your treament may affect your ability to obtain or retain a clearance, even if they are legitimately prescribed drugs. Many government jobs hinge on the ability to obtain and keep a clearance. If this is the case, it will (or should) clearly state in your offer letter that "employment is contingent upon passing a drug test and the ability to obtain and retain a clearance" or something along that line.
Generally, if the treatment was for depression that didn't cause you to harm yourself or others or didn't cause behavior which may compromise security, you should be OK. The company will probably talk to your health care provider and ask them if they feel confident that you are able to carry out your job duties without or the security of the project.
Good luck with your job and I hope this has helped.
I really understand your problem,I was told I could start a job working in the medical field on a Thursday two years ago. I took my drug test which was fine except for my meds.I kept calling the lady back and all they ever said was we are waiting on your labwork. After 3 times of hearing this I knew I had lost the job. Its sad,but hang in there. Not all companies are as narrowed minded. Good Luck!
Wow- that's really awful. A total invasion of privacy.Don't be anxious (if you can help it) try to present a cool, calm, capable exterior. The Focus should be that you are dealing with the issue, that you take it seriously, and are working to remedy it. You are well-spoken, and obviously intelligent. You are qualified. Deal with every challenge they put before you with an air of confidence. Be mindful of your body language- present as relaxed. Try not to let your mind get ahead of you -you can see your thoughts racing in what you wrote -"What if",etc. deal with issues as they arise. Good luck- you can do it!
If you are Bipolar; Say good bye to LIFE Insurance and many other forms of Insurance.
With that in Mind, If This company feels you are a liability KISS the Job GOOD BYE!
IMHO- Always submit to drug tests, Don't give information away. Don't tell anyone about your possible mental disorder! They test for known substance abuse, not pyhsciatric medication. The tests involved in finding your meds are specific and will most likely not show up on a normal drug test for a JOB.
LEARN TO ANSWER QUESTIONS SPECIFICALLY. Only give information that is required, NO MORE!
Source(s):
10 years Bipolar... I have had 6 jobs in the past 10 years.... My current job is 14months old.lets hope it lasts ;)
i think you could check with the ADA office in your city to learn your rights
I applied for a job and had to sign a medical and I had to be careful how I worded the fact that I am on meds for stress related issues and keep the word bipolar out of it. In 2000 I applied for a job and had to get a doctors report filled out. My doctors verified that I was meds and that I was in good health and would cause no threat to those around me and I still got the job. They should not discrimminate but I'm sure it happens in the guise of some other lame excuse.
Absolutely. Ask any military recruiter. Look at it like this - if you need to be medicated in order to deal with plain old life, you certainly do not need to be placed in situations that entail high stress, high levels of responsibility, or life and death at the taxpayer's expense. "Stablilized on medication" means YOU CAN NOT or WILL NOT deal with life unless you are medicated. Sorry, but as a taxpayer and a soldier, I don't want ya in the foxhole.
Consider also, you have what is called a "pre-existing condition", that you will expect to be covered by their medical insurance. That could get very expensive for them, so from solely a financial standpoint, the answer would be that they are not interested in hiring you. This doesn't even begin to cover the fact that your "condition" means you are more likely to take time off, and I am sure you know time is money to any corporation.
So, is all this politically correct? No. But is IS how things are done. Sorry.
job discimination is illegal
Source(s):
I wacth tv alot
Be honest.
NR1 Psychiatric and Substance-Use Disorders in an Advanced HIV Minority Cohort
Mubasher Naseer, M.A., Department of Pathology, Mount Sinai Medical Center, One Gustave Levy Place, New York, NY 10029-6574; Amy I. Tal, M.S., Jennifer G. Monzones, B.A., Elizabeth L. Ryan, Ph.D., Susan Morgello, M.D.
At the conclusion of this session, the participants will have a greater understanding of the high prevalence of psychiatric and substance use disorders among this population. Concomitant diagnoses of substance use and mood disorders will be demonstrated. A need for greater vigilance to such pathology in diverse populations will be elucidated.
Objective: While the prevalence of HIV has skyrocketed among minorities, research on the rates of psychiatric disorders among these individuals is scant.
Method: We report rates of disorders among an advanced HIV inner-city cohort (the Manhattan HIV Brain Bank) who were evaluated every six months via a semi-structured psychiatric interview (PRISM). The sample consisted of 209 patients (76% men) who were mostly minority (42% Black, 33% Hispanic).
Results: The most prevalent lifetime disorder was MDD (65%), with other diagnoses at much lower rates (i.e., Dysthymia: 16%, PTSD:15%, Mania: .009%). Similar patterns emerged for current psychiatric disorders, albeit at lower rates. Substance use disorders (SUDS) were comparable or exceeded psychiatric diagnoses. The most frequent lifetime dependence diagnoses were Cocaine (61%), Opiates (45%), Alcohol (43%), and Cannabis (19%). Rates for current dependence were high but lower than for lifetime. Urine toxicology results identified additional current substance users. Only 18% of the cohort was free of any SUD.
Conclusions: Rates of SUDS and psychiatric disorders are greater than those previously reported. Our results confirm the feasibility of using a semi-structured interview with an advanced HIV inner-city cohort and indicate exceedingly high rates of psychiatric disorders. Implications for treatment and psychiatric comorbidity will be discussed. 1. Bing EG, Burnam MA, Longshore D, Fleishman JA, Sherbourne CD, London AS, et al. (2001). Psychiatric disorders and drug use among human immunodeficiency virus-infected adults in the United States. Archives of General Psychiatry, 58, 721-728. 2. Ferrando S, Goggin K, Sewell M, Evans S, Fishman B, & Rabkin J, (1997). Substance use disorders in gay/bisexual men with HIV and AIDS. The American Journal on Addictions, 7, 51-60.
NR2 Dopaminergic Challenge in Adolescents With ADHD and Nicotine Dependence
Himanshu P. Upadhyaya, M.B., Psychiatry, Medical University of South Carolina, 1159 Sea Eagle Watch, Charleston, SC 29412; Wei Wang, M.D., Kathleen T. Brady, M.D.
At the conclusion of this session, the participant should be able to learn about the involvement of dopaminergic system in adolescents with nicotine dependence. Introduction: Dopaminergic systems are involved in the pathophysiology of attention deficit hyperactivity disorder (ADHD) and nicotine dependence. However, there is a lack of research examining the dopaminergic systems in adolescents with ADHD and nicotine dependence. We present preliminary results from a study examining the dopaminergic systems in adolescents with ADHD, and nicotine dependence.
Methods: Thirty-five participants (15 - 20 yr.) were recruited. Neuroendocrine and behavioral response to the dopaminergic agents- methylphenidate (10 mg) and pramipexole (0.25 mg) were examined. Measures of these responses were spontaneous eye-blink rate, plasma prolactin (PRL), and growth hormone (GH). Additionally, participants completed a visual analog mood scale (VAMS).
Results: Adolescents with nicotine dependence had a blunted growth hormone response and greater VAMS “euphoric”, as well as “energized” response to methylphenidate as compared to controls. Nicotine dependent participants also had a greater VAMS “engergized” response to pramipexole as compared to controls.
Conclusion: Adolescents with nicotine dependence may have a blunted dopaminergic activity as compared to controls. Implications of the results will be discussed. 1. Di Chiara G. Role of dopamine in the behavioural actions of nicotine. related to addiction. European Journal of Pharmacology 2000; 393:295-314. 2. Solanto MV. Dopamine dysfunction in AD/HD: integrating clinical and basic neuroscience research. Behavioural Brain Research 2002; 130:65-71.
NR3 ADHD, Treatment, and Substance Use Pattern in College Students
Himanshu P. Upadhyaya, M.B., Psychiatry, Medical University of South Carolina, 1159 Sea Eagle Watch, Charleston, SC 29412; Kathleen O’Rourke, Ph.D., Kelly Rose, B.A., Wei Wang, M.D., Brian Sullivan, Psy.D., Kathleen T. Brady, M.D.
At the conclusion of this session, the participant should be able to learn about substance use patterns among college students with ADHD. Introduction: The objective of this preliminary study was to examine ADHD treatment and substance use pattern among college students.
Methods: Three hundred and thirty four (334) older adolescents at a local college were surveyed about current ADHD symptoms and psychopharmacological treatment. The survey was conducted in conjunction with the annual CORE survey that explores the student’s substance use patterns and attitudes.
Results: Participants with current ADHD symptoms were more likely to initiate cigarette smoking earlier (p=0.04), and have higher use of cigarettes (p=0.034) and “other” drugs (p=0.003) in the preceding year as compared to those without current ADHD symptoms. Participants on medication, with current ADHD symptoms, were more likely to use “other drugs” in the past month (p = 0.009) and tended to use more tobacco in the past year (p = 0.077) as compared to those without current ADHD symptoms. A significant minority of the participants reported abuse/diversion of their medication for recreational use.
Conclusion: Results of our preliminary study indicates that adequate symptom control for ADHD may be important to reduce substance use among college students with ADHD. Further prospective studies in this population are warranted to examine the relationship between ADHD treatment, substance use, and medication abuse/diversion. 1. Barkley RA, Fischer M, Smallish L, et al. Does the treatment of attention deficit/hyperactivity disorder with stimulants contribute to drug use/abuse? A 13-year prospective study. Pediatrics 2003; 111:97-109. 2. Wilens TE, Faraone SV, Biederman J, et al. Does stimulant therapy of attention-deficit/hyperactivit. disorder beget later substance abuse? A meta-analysis review of the literature. Pediatrics 2003; 111:179-185.
NR4 Ecstasy Use in the U.S. and Its Relationship With Other Drug Use and Dependence
Silvia S. Martins, M.D., Mental Health Department, Johns Hopkins School of Public Health, 624 N. Broadway, PO Box 671, Baltimore, MD 21205-1900; Guido Mazzotti, M.D., Howard D. Chilcoat, Sc.D.
At the conclusion of this session, the participant should be able to recognize patterns of ecstasy users in USA and the association of ecstasy use with other drug use and dependence.
Background: Ecstasy use presents increasing trends in USA. Little is know about its natural history and its relationship with other drugs abuse. Objectives: To compare chronic versus new ecstasy users and marijuana users by lifetime drug use and dependence.
Method: Secondary analysis from the 2001 National Household Survey on Drug Abuse (n= 5,561 respondents). Data were matched using binary logistic regression models performed with STATA 8.0.
Results: Prevalence of ecstasy use was higher for males and whites. Marijuana use typically preceded ecstasy use which preceded cocaine/heroin use. Chronic ecstasy users were more likely to use cocaine, crack, heroin, LSD, inhalants, tranquilizers, stimulants and sedatives (ORs³3.97); be alcohol dependent (OR=3.27), cocaine dependent (OR=4.78) and heroin dependent (OR=5.93) compared to new users. Ecstasy users were more likely to use cocaine, inhalants, tranquilizers and stimulants versus marijuana users (ORs³1.44). Chronic ecstasy users were more likely to be cocaine dependent (OR=1.73) and heroin dependent (OR=2.15) than marijuana users.
Conclusion: Chronic ecstasy users have higher occurrence of other drug use and dependence than recent onset ecstasy users and marijuana users. These findings suggest early intervention for ecstasy users can potentially attenuate the progression to multiple use or dependence of drugs. 1. Pedersen W, Skrondal A. Ecstasy and new patterns of drug use: a normal population study. Addiction, 94 (11), 1695-1706, 1999. 2. Topp L, Hando J, Degenhardt L, et al. Ecstasy use in Australia: patterns of use and associated harm. Drug Alcohol Depend, 55, 105-15, 1999
NR5 Bipolar Disorder, Substance Abuse, and Antidepressant-Induced Mania
Sumita G. Manwani, M.D., Psychiatry Department, Cambridge Hospital, 1493 Cambridge Street, Cambridge, MA 02139; Tamara B. Pardo, B.A., S. Nassir Ghaemi, M.D.
At the conclusion of this session, the participant should be able to study whether substance use disorders are a potential risk factor for antidepressant induced mania in bipolar patients.
Objective: Substance use disorder (SUD) has been associated with increased risk for antidepressant-induced mania (ADM) in bipolar disorder (1). This analysis seeks to confirm these findings, and identify other predictors of ADM (2).
Method: In a partial data analysis, we examined 108 trials in 30 bipolar disorder patients involving SUD (n=65) and no SUD (n=43). The full data analysis of about 400 trials will be presented.
Results: Crude rates demonstrated no notable difference in risk of ADM in SUD patients (19.3%) vs. non-SUD patients (25.6%) (p=0.71). Adjusted for potential confounders (age, gender, type of substance, number years ill, number of MDEs, number manic/hypomanic episodes, number AD trials total, and type of AD), logistic regression again reveals no notable impact of SUD for ADM risk (OR=1.37, [0.04, 47.2]). History of >10 past manic/hypomanic episodes was the main ADM predictor (OR=15.2, [1.03, 224.7]; 29.8% in high manic/hypomanic episode group vs. 11.9% in low episode group). Interestingly, among specific substances, the main observation was decreased ADM risk with cocaine abuse (OR=0.008, [0.0001, 0.48]; 7.7% in cocaine abusers vs. 24.1% in non-abusers).
Conclusions: SUD may not increase risk of ADM, but >10 past manic/hypomanic episodes may be a major ADM predictor. 1. Goldberg JF, Whiteside J. The association between substance abuse and antidepressant-induced mania in bipolar disorder: a preliminary study. J Clin Psychiatry 2002; 63:9:791-795. 2. Henry C, Sorbara F, Lacoste J, Gindre C, Leboyer M. Antidepressant-induced mania in bipolar patients: identification of risk factors. J of Clin Psychiatry 2001; 62:249-255.
NR6 Defense Mechanisms in Patients With Panic Disorders Before and After Cognitive-Behavioral Therapy
Gisele G. Manfro, M.D., Department of Psychiatry, HCPA, Luiz Manoel Gonzaga 630/11, Porto Alegre, RS 90470-280, Brazil; Carolina Blaya, M.D., Elizeth Heldt, Leticia Kipper, Luciano Isolan
At the conclusion of this session, the participant should be able to recognize that panic disordered patients use maladaptative defense mechanisms according to DSQ-40 and that these patients use less neurotic defense mechanisms after achieving remission with CBT. Defense mechanisms are used to evaluate psychodynamic functioning and are an important dimension of the structure of personality. Studies have demonstrated that patients with panic disorder (PD) use a more maladaptive pattern of defense mechanisms, but there is little data involving the study of the use of these mechanisms during the symptomatic stage and after PD remission. The aim of this study is to evaluate the defense mechanisms used by patients with PD refractory to medication treatment and to verify whether the use of these mechanisms modify with the augmentation of cognitive-behavioral therapy.
Methods: Twenty-nine panic disordered patients, according to the DSM-IV criteria, participated in the study. The M.I.N.I. was used to perform the diagnostic evaluation of patients. The severity of the panic disorder was evaluated by the C.G.I. and by the Panic Inventory. The defense mechanisms were evaluated by the DSQ-40 (Defense Style Questionnaire). The instruments were applied at the baseline and after 12 session cognitive-behavioral group therapy.
Results: Patients decrease the use of neurotic defenses (5.1 vs. 4.7, p=0.04) and there is a trend to decrease immature defenses (4.6 vs. 4.2, p=0.07) with CBT. Remission (CGI £ 2 and no attacks) influences the differences in the use of neurotic mechanisms (p=0.04).
Conclusion: Panic disordered patients use less maladaptative defenses after achieving remission with CBT. 1. Heldt E, Manfro GG, Kipper L, Blaya C, Maltz S, Isolan L, Hirakata VN, Otto MW: Treating Medication-Resistant Panic Disorder: Predictors and Outcome of Cognitive-Behavior Therapy in a Brazilian Public Hospital. Psychother Psychosom 2003; 72:43-48. 2. Leichsenring F, Lei bing E. The Effectiveness of Psychodynamic Therapy and Cognitive Behavior Therapy in the treatment of Personality Disorders: A Meta-Analysis. Am J Psychiatry 2003; 160:1223-1232.
NR7 Comorbidity of Anxiety Disorders in a Community Setting
Matthew G. Biel, M.D., Psychiatry Department, New York University, 214 Mulberry Street, Apt. 6E, New York, NY 10012; Brady G.S. Case, M.D., Eric D. Peselow, M.D., Mary Anne Pressman, M.D., Mary T. Guardino, B.A.
At the conclusion of this session, the participant should be able to understand the frequency of comorbidity among the various anxiety disorders and depression so we can get a better understanding of treating these disorders.
Objective: The purpose of this paper is to evaluate the comorbidity of all of the anxiety disorders with other anxiety disorders (OCD, social & specific phobias, generalized anxiety disorder) & depression, in order to assess frequency of comorbid diagnosis.
Method: Over the past 10 years, at the Freedom from Fear Clinic in Staten Island N.Y. (an outpatient anxiety disorder clinic associated with Columbia University) we have evaluated 706 patients who were primarily diagnosed with either panic disorder, OCD, social phobia, generalized anxiety disorder or depression using a modified symptom check list adapted from the SCID during the acute stage of the illness.
Results: Overall only 63 of the 213 patients (29.6%) of the sample met criteria for a single diagnosis (one of the four other anxiety disorders or depression). 142 of the 213 patients met criteria for panic with agoraphobia (66.7%). Comorbidity of panic was as follows: Panic with other anxiety disorders or depression196/255(76.9%) Depression with other anxiety disorders192/281 (68.2%) Social phobia other anxiety disorders or depression28/48 (58.3%) OCD other anxiety disorders or depression57/90 (63.3%) GAD other anxiety disorders or depression27/32 (84.4%)
Conclusions: Overall the diagnosis of anxiety disorders was associated with a high rate of comorbidity. The greater the number of anxiety diagnoses the poorer the response to treatment of the panic disorder. Implications of these findings will be discussed. 1. Barlow DH, DiNardo PA, Vermilyea BB, Vermilyea J, Blanchard EB: Comorbidity and depression among the anxiety disorders. J Nerv ment Disord, 174, 63-72, 1986. 2. Stein MB, Tancer ME, Uhde TW. Major depression in patients with panic disorder: factors associated with course and recurrence. Journal of Affective Disorders, 19, 87-296, 1990.
NR8 GAD in General Practice in the Nordic Countries: Conspicuous and Hidden
Supported by Wyeth Pharmaceuticals Povl Munk-Joergensen, Aalborg Psychiatric Hospital, Molleparkvej 10, Aalborg, DK 9000, Denmark; Ib Rasmussen, M.D., Christer Allgulander, M.D., Alv A. Dahl, M.D., Anti Virta, Martin Holm, Leslie Folager
Approximately 50% of the frequent disorders such as depression, anxiety, and somatisation remain unrecognized to the general practitioner. The purpose of the study is to estimate the prevalence of GAD in general practices in the Nordic countries (Denmark, Finland, Norway, and Sweden), determine the rate conspicuous/hidden and identify predictors for recognition. 656 general practitioners (GP) from the four Nordic countries participated in the study. GP filled in a schedule characterizing the practice and the doctor, the patient filled in a questionnaire about symptomathology, depression, and other studies Generalized Anxiety Screening Questionnaire (GAS-Q), and depression, Depression Screening Questionnaire (DSQ) making it possible to diagnose GAD and other anxiety disorders, and major depression according to DSM IV criteria. The general practitioner filled in a schedule Generalized anxiety and Depression in Primary care (GAD-P) giving his/hers statement about patients mental disorders (if any) not knowing the result of the patients schedule. 8879 patients participated in the study, 471 were identified as meeting the full GAD criteria. Overall GAD prevalence was 5,6 % (4,7% - 6,4%). Identification rate was overall 37,9% (range 33,8% - 53,2%). Important predictors for identification were: Patient subjective feeling of anxiety, depression, impairment by psychological problems and worries unable to handle. Predictors are analysed in a multi variant statistical model. Identification of GAD in general practice may be improved by focusing on Patient subjective feeling of anxiety, depression, impairment by psychological problems and worries unable to handle.
NR9 State-Trait Anxiety and Anxiety Sensitivity in Predicting 35% Carbon Dioxide Response
Emel S. Monkul, M.D., Department of Psychiatry, UTHSCSA, 7703 Floyd Curl Drive, San Antonio, TX 78229; John P. Hatch, Ph.D., Elif Onur, M.D., Tunc Alkin, M.D., Umit Tural, M.D., Huray Fidaner, M.D.
At the conclusion of this session, the participant should be able to recognize the difference between anxiety sensitivity and state and trait anxiety, and the effects of these on the response to 35% CO2 challenge.
Objective: The aim of this study was to examine the effects of state-trait anxiety and anxiety sensitivity on response to a CO2 challenge in panic disorder patients (PD), their healthy first-degree relatives (HR) and healthy controls (HC).
Methods: Our sample consisted of 32 DSM-IV PD, 32 HR and 34 HC. We used air (placebo) and a mixture of 35%CO2/65%O2. Anxiety Sensitivity Index (ASI) and State-Trait Anxiety Inventory for subjective anxiety and Panic Symptom List for panic symptoms were used. A CO2-induced panic attack was defined by an increase from baseline >1 points in at least 4 panic symptoms, at least one being a cognitive symptom.
Results: PD had increased anxiety sensitivity and state-trait anxiety scores compared to HR and HC (ANOVA, p<0.001); the difference between HR and HC was not significant. A past history of suffocation increased the risk of CO2 reactivity (Odds ratio=3.13, CI=1.196-8.201) in the whole group. In female PD high ASI and trait anxiety predicted CO2-induced panic (logistic regression analysis, p<0.05).
Conclusions: ASI seems to have a gender-specific relation to CO2 reactivity. History of suffocation might be an important predictor of CO2-induced panic. This work was partly supported by an award from Turkish Psychiatric Association, Izmir Branch. 1. van Beek N, Griez: Reactivity to a 35% CO2 challenge in healthy first-degree relatives of patients with panic disorder. Biol Psychiatry 2000; 47:830-835. 2. van Beek N, Griez E: Anxiety sensitivity in first-degree relatives of patients with panic disorder. Beh Res Ther 2003; 41:949-957.
NR10 Changes in Biofeedback Variables After Pharmacotherapy in Panic Disorder
Bum-Hee Yu, M.D., Department of Psychiatry, Samsung Medical Center, 50 Ilwon-Dong, Gangnam-Gu, Seoul 135-370, Korea; Moon S. Koo, M.A.
At the conclusion of this session, the participant should be able to understand the relationship between anxiety and biofeedback variables in panic disorder understand the availability of EDR as a sensitive index to reflect treatment response in panic disorder.
Objective: Anxiety has been known to be related with some pathophysiologic variables. This study aimed to find the changes in the biofeedback variables after pharmacotherapy.
Method: We recruited 38 panic patients (M:25 F:13, according to the DSM-IV) at the Samsung Medical Center in Seoul and 33 normal control subjects (M:21 F:12). Panic patients were treated with paroxetine. All subjects were assessed both at the beginning of the study and 3 months after pharmacotherapy. We measured forearm EMG, frontal EMG, electrodermal response (EDR), and body temperature using the Procomp & Biograph biofeedback instrument. Hamilton Anxiety Rating Scale (HAM-A), Hamiltone Depression Rating Scale (HAM-D), Beck Depression Inventory (BDI), Spielberger State and Trait Anxiety Inventory (STAI-S, STAI-T) and Acute Panic Inventory(API) were also measured.
Result: Panic patients showed higher baseline EDR (p=0.033), compared with normal control subjects. Panic patients showed higher scores on HAM-A, HAM-D, BDI, STAI-S, STAI-T, and ASI. (all p values<0.001). After 3 months of pharmacotherapy, panic patients improved on baseline EDR (p=0.016), stress EDR (p=0.021), and recovery EDR (p=0.004), and showed significant improvement in HAM-A, HAM-D, BDI, STAI-S, STAI-T, ASI, and API. (all p-values <0.001)
Conclusion: EDR measured by the biofeedback instrument decreased after pharmacotherapy in panic disorder. Thus, EDR may be a sensitive index to reflect treatment response in panic disorder. 1. Scheibe G, Nutzinger D, Buller R, Walther AU. 1992. Pretreatment anxiety level as differential predictor in outpatients with panic disorder. Arzneimittelforschung 42: 1090-1094. 2. Bernhard R. Slaap MA, and Johan A. den Boer, M.D., Ph.D. 2001. The prediction of nonresponse to pharmacotherapy in panic disorder: A review. Depression and anxiety 14; 112-122(2001)
NR11 An Efficacy Comparison of Atypical Antipsychotic Medications for PTSD
Naomi M. Mendelovicz, M.D., Psychiatry Department, Dartmouth Medical School, One Medical Center Drive, Lebanon, NH 03756; Bradley V. Watts, M.D., David H. Rubin, M.D., Rebecca L. Hirsch, M.D., Keith R. Warren, M.D., Bradley A. McLure, M.D., Lorna K. Mayo, M.D.
At the conclusion of this presentation, the participants should demonstrate an understanding about the comparative efficacy of atypical antipsychotic medications for posttraumatic stress disorder.
Objective: There is accumulating evidence regarding the use of atypical antipsychotic medications for treatment of post-traumatic stress disorder (PTSD). There are no trials that compare the efficacy of these agents. This project seeks to compare the efficacy of atypical antipsychotic agents in treatment of PTSD.
Method: A retrospective chart review was performed on 982 patients diagnosed with PTSD treated in the outpatient mental health clinic at the White River Junction VA Medical Center in 2001. The global assessment of function scores (GAF) for patients starting treatment with an atypical antipsychotic medication was obtained.
Results: Nineteen percent of patients with PTSD in the outpatient clinic received an atypical trial during 2001. Of those, 54% were treated with quetiapine, 26% with olanzapine, and 19% with risperidone. The average change in GAF score was 4.9 for quetiapine, 4.6 for olanzapine, and 3 for ripseridone. Each agent showed statically significant change in mean GAF from baseline. There was no significant difference in the mean change or percent of patients improved between any agents.
Conclusions: Atypical antipsychotic agents were commonly used in this patient population to treat PTSD. Each medication showed statistically significant improvement in GAF scores. There was no significant difference in the efficacy comparing agents. 1. Harel TZ, Smith DW, Rowles JM: A comparison of psychiatrists’ clinical-impression based and social workers computer-generated GAF scores. Psych Services 2002; 53:340-2. 2. Albucher RC, Liberzon I: Psychopharmacological treatments of PTSD: a critical review. J Psych Research 2002; 36:355-67.
NR12 Skin Picking: A Symptom Across Multiple Diagnoses
Dena C. Rabinowtiz, Ph.D., Bio-Behavioral Institute, 935 Northern Boulevard, Suite 102, Great Neck, NY 11021; Fugen Neziroglu, Ph.D., Matthew Jacofsky, M.A., Anna Breytman, Ph.D., Jose A. Yaryura-Tobias, M.D.
At the conclusion of this session, the participant should be able to recognize skin picking due to increased awareness of related behaviors and emotions linked to this symptom. Participants should also be able to identify important aspects of skin picking behavior as it is related to different psychiatric diagnoses and treatment.
Objective: Although skin picking behavior is observed in numerous diagnostic entities such as Body Dysmorphic Disorder, Obsessive-Compulsive Disorder, Trichotillomania, and Borderline Personality Disorder, it has received relatively little attention in the psychological literature. The current study sought to examine descriptive details about skin picking behavior.
Method: Thirty participants who reported that they engage in skin picking completed self-report questionnaires assessing demographic, symptom, and diagnostic information.
Results: Participants ranged from ages 19-77 and 70% of participants were women. Overall, participants reported that they experienced negative feelings prior to picking such as anxiety, loss of control, tension, and general negative mood. After picking, participants did not report a substantial reduction in these emotions but an increase in intensity and types of negative mood states including shame, guilt, and physical pain. Information regarding location, triggers, and implements for picking, frequency, duration and level of interference was also gathered.
Conclusion: The findings offer new information about skin picking behavior and offer a behavioral analysis of this often neglected symptom. Implications for diagnosis, treatment, and relevance in Body Dysmorphic Disorder are also addressed. 1. Neziroglu F, Mancebo M: Skin picking as a form of self injurious behavior. Psychiatric Annals 2001; 31:549-555. 2. Yaryura-Tobias JA, Mancebo M, Neziroglu F: Clinical and theoretical issues in self injurious behavior. Rev Bras Psiquiatr 1999; 21:178-183.
NR13 ADHD Comorbidity and Gender Differences in Children
Anela Bolfek, M.D., Psychiatry Department, Tufts - NEMC, 750 Washington Street, 1007, Boston, MA 02111; Atilla Turgay, M.D., Rubaba Ansari, M.A., David Ng, M.D.
At the conclusion of this session, insight into the nature and frequency of comorbid disorders in ADHD - differentiate gender differences in ADHD comorbidities
Objective: Most attention-deficit/hyperactivit. disorder (ADHD) studies are based on small samples, which do not provide reliable information on gender differences and comorbidities in specific age groups. This study with 1655 patients provided more reliable information.
Methods: The patients were diagnosed according to DSM-IV criteria, DuPaul ADHD Rating Scale, and Offord-Boyle Child Health Study parent and teacher rating scales. Sample: The patient sample consisted of 1318 (79.64%) males and 337 (20.36%) females, 6-12 years of age. They were seen in a university hospital, ADHD clinic, training and research institute.
Results: Most patients (77.89%) suffered from two or more disorders. Oppositional Defiant Disorder, Conduct Disorder, and Anxiety Disorders were most common (60.36%, 19.27%, 11.30% respectively). Also observed were Dysthymic Disorder, Pervasive Developmental Disorders, and Major Depression (4.05%, 3.50%, 2.30% respectively). A greater number of males were observed in any given comorbidity (ratios ranged from 3.2:1 to 5.5:1). However, females were more likely to have comorbid Anxiety Disorders or Dysthymic Disorder than males (13.35% vs. 10.77%, 5.04% vs. 3.79% respectively).
Conclusion: It is highly likely that an ADHD patient will develop other disorders. ADHD patients should be carefully screened for other comorbidities, for which additional medications may be required. 1. Lalonde J, Turgay A, Hudson J.I. (1998): Attention-deficit hyperactivity disorder subtypes and comorbid disruptive disorders in a child and adolescent mental health clinic. Can J Psychiatry 43:623-628 2. Turgay A, Urdaravic V, Ansari R, Oncu B, Erman O (2002): Tic disorder in children and adolescents with ADHD. Abstract in print for Pediatric Child Health, the Canadian Pediatric Society Journal, June issue 3. Turgay A, Erman O, Oncu B, Ansari R, Urdarevic V (2002): Comorbidities in conduct disorder may determine the type of medication treatment. Abstract in print for Pediatric Child Health, the Canadian Pediatric Society Journal, June issue
NR14 Suicidality in Depressed Patients With and Without a History of Alcoholism
Leo Sher, M.D., Department of Psychiatry, Columbia University, 1051 Riverside Drive, Suite 2917, Box 42, New York, NY 10032; Maria A. Oquendo, M.D., Hanga G. Galfalvy, Ph.D., Michael F. Grunebaum, M.D., Ainsley K. Burke, Ph.D., J. John Mann, M.D.
At the conclusion of this session, participants should be able to identify risk factors for suicidal behavior in depressed patients with a history of alcoholism. Introduction: Studies suggest that depressed subjects with a history of alcoholism have more chronic impairment and higher suicidality than individuals with either diagnosis alone. We hypothesized that smoking and aggression contribute to higher suicidality in depressed subjects with a history of alcoholism compared to depressed subjects without a history of alcoholism.
Methods: Two hundred nineteen depressed subjects without a history of any alcohol or substance abuse/dependence and 129 depressed individuals with a history of alcohol abuse/dependence participated in the study. All subjects were free from alcohol or substance abuse for at least 2 months. Demographic and clinical parameters were assessed and recorded.
Results: The logistic regression analysis indicates that higher prevalence of suicide attempters in the group with a history of alcoholism compared to the group without a history of alcoholism is related to higher aggression scores in the former group. Higher suicide ideation scale scores in depressed subjects with a history of alcoholism is related to higher prevalence of smoking and higher aggression scores in this group compared to the other group.
Conclusions: Our findings suggest that in addition to obtaining a history of depression and suicidal behavior, clinicians should assess comorbidity with alcoholism and cigarette smoking, and personality features such as aggression. 1. Sher L, Oquendo MA, Li S, Huang YY, Grunebaum MF, Burke AK, Malone KM, Mann JJ. Lower CSF homovanillic acid levels in depressed patients with a history of alcoholism. Neuropsychopharmacology 2003; 28:1712-1719. 2. Cornelius JR, Salloum IM, Mezzich J, Cornelius MD, Fabrega H Jr, Ehler JG, Ulrich RF, Thase ME, Mann JJ. Disproportionate suicidality in patients with comorbid major depression and alcoholism. Am J Psychiatry 1995; 152:358-364.
NR15 QEEG and P300 in Patients With Hepatoencephalopathy
Sang-Ick Han, M.D., Department of Neuropsychiatry, Out Lady of Mercy Hospital, 665 Pupyung-Dong, Pupyung-Gu, Inchon 403-720, South Korea; Wan-Seok Yang, M.D., Yang-Whan Jeon, M.D.
At the conclusion of this session, the participant should be able to recognize that the alpha band analysis of quantitative electroencephalogram and auditory and visual P300 could be useful for exploring the cognitive dysfunctions in patients with hepatic encephalopathy.
Objective: Digitalized quantitative electroencephalogram (QEEG) and P300 event-related potentials (ERP) were used to detect mild cognitive dysfunctions at the early phase in patients with hepatic encephalopathy.
Method: Digitalized QEEG and auditory and visual “oddball” paradigm P300 were employed in normal controls (N=6) and patients with hepatic encephalopathy (N=6). EEG activity was recorded from 25 electrodes, referred to nose. Auditory stimulus categories were defined as the standard (1000 Hz, 80%) and target (2000 Hz, 20%) with the intensity of 75dB. Visual stimulus categories were defined as the standard (circle, 3.5 cm diameter, 80%) and target (square, 15 cm on a side, 20%). The stimuli were presented in random series, once every 2 seconds.
Results: The dominant alpha was smaller and lower in patients with hepatic encephalopathy in occipital areas (F=10.7, P<0.01). P300 was delayed (F=16.8, P<0.01) and smaller (F=17.1, P<0.01) across both auditory and visual modalities in patients with hepatic encephalopathy. Visual P300 was more delayed than auditory P300 in patients with hepatic encephalopathy (F=12.4, P<0.01), but not smaller (F=1.9, n.s.).
Conclusions: QEEG and P300 ERPs, especially visual P300 latency, could be used as an early detector for mild brain dysfunctions in patients with hepatic encephalopathy. 1. Hollerbach S, Kullmann F, Frund R, Lock G, Geissler A, Scholmerich J, Holstege A: Auditory event-related cerebral potentials (P300) in hepatic encephalopathy--topographic distribution and correlation with clinical and psychometric assessment. Hepatogastroenterology 1997; 44:1002-1012 2. Davies MG, Rowan MJ, MacMathuna P, Keeling PW, Weir DG, Feely J: The auditory P300 event-related potential: an objective marker of the encephalopathy of chronic liver disease. Hepatology 1990;12:688-694
NR16 P300 in Patients With Brain Concussion
Sang-Ick Han, M.D., Department of Neuropsychiatry, Out Lady of Mercy Hospital, 665 Pupyung-Dong, Pupyung-Gu, Inchon 403-720, South Korea; Wan-Seok Yang, M.D., Yang-Whan Jeon, M.D.
At the conclusion of this session, the participant should be able to recognize that P300 could be useful for exploring cognitive dysfunctions in patients with brain concussion.
Objective: Although abnormal MRI findings were not shown in patients with brain concussion by traffic accidents, it has been well known that their cognitive dysfunctions could be complained. This study was design to examine the availability of P300 as an objective measure reflecting minor brain dysfunctions.
Method: Auditory and visual “oddball” paradigms were employed in normal controls (N=12) and patients with brain concussion without MRI abnormalities (N=12). Auditory stimulus categories were defined as the standard (1000 Hz, 80%) and target (2000 Hz, 20%) with the intensity of 75dB. Visual stimulus categories were defined as the standard (circle, 3.5 cm diameter, 80%) and target (square, 15 cm on a side, 20%). The stimuli were presented in random series, once every 2 seconds.
Results: P300 in patients with brain concussion was elicited later (F=14.4, P<0.001) and smaller (F=45.8, P<0.0001) across the both auditory and visual modalities. There were no interactions groups (controls vs. patients) and modalities (auditory vs. visual) in P300 latency (F=0.2, n.s.) and in P300 amplitude (F=0.3, n.s.).
Conclusions: Even though brain lesion was not shown by MRI in patients with brain concussion, the subtle cognitive dysfunctions could be detected by both auditory and visual P300. 1. Keren O, Ben-Dror S, Stern MJ, Goldberg G, Groswasser Z: Event-related potentials as an index of cognitive function during recovery from severe closed head injury. J Head Trauma Rehabil 1998; 13:15-30 2. Sangal RB, Sangal JM: Closed head injury patients with mild cognitive complaints without neurological or psychiatric findings have abnormal visual P300 latencies. Biol Psychiatry 1996; 38:305-307
NR17 One ECT Session Is Not Sufficient to Produce Memory Dysfunction: A Controlled Study
Lorena Rami-Gonzalez, Ph.D., Department of Psychiatry, Hospital Clinic, Villarroel, Barcelona, Spain; Javier Goti, Teodor Marcos, Ph.D., Miguel Bernardo, M.D., Maria J. Portella, M.S.C., Manel Salamero, M.D.
At the conclusion of this session, the absence of memory impairment after one M-ECT session reinforce the efficiency of this treatment and would perhaps facilite the inclusion of patients in M-ECT programs.
Background: Memory dysfunction is one of the main adverse effects of ECT treatment. Information consolidation and retrieval depend on the medial temporal lobe and on hippocampal-diencephalic functional circuits. These areas are the most predisposed to unchain massively Long Term Potentiation (LTP) neuronal plasticity phenomenon. The massive LTP induction has been proposed as a neurophysiological bases of the memory disorders by ECT. Aim: To know if one ECT session may be sufficient to unchain neurophysiological mechanisms to produce significant memory impairment.
Method: Twenty-four psychiatric outpatients treated with M-ECT. Twelve patients were assessed before and nineteen minutes after an ECT session. Twelve patients treated with M-ECT were used as control group and were assessed when they arrived at the hospital and nineteen minutes after, just before ECT session.
Results: Experimental group do not show a marked shift in cognitive functions in the second test session. Groups only differed significantly in visuospatial test F (1, 18) = 7.04, P = 0.015.
Conclusions: One M-ECT session may not permit massive LTP and NMDA receptors dysfunction to produce memory or other cognitive dysfunction. Otherwise, we found a visuospatial dysfunction, suggesting that one ECT may implicate an asymmetrical transitory dysfunction on right hemispheric. 1. Stewart C, Jeffrey K, Reidl (1994). LTP-like synaptic efficacy changes following electroconvulsive therapy. Annals New York Academy of Sciences, 462:307. 2. Rogers MA, Bradshaw JG, Phillips JG et al. (2002). Attentional asymmetries following ECT in patients with major depression. Neuropsychologia, 40:241-44.
NR18 Tau-Protein and Beta-Amyloid as Diagnostic Markers of Alzheimer’s Dementia
Vladimir Pidrman, M.D., Psychiatry Department, University Hospital, I.P. Pavlova 12, Olomouc, CZ 77520, Czech Republic; Klara Latalova, Jiri Mares, M.D., Karel Urbanek, M.D.
At the conclusion of this session, the examinations of tau-protein and beta-amyloid levels (in cerebrospinal liquor) may be suitable for diagnostic Alzheimers dementia and eliminating vascular dementia. Assumption: Changes levels of tau protein (inceasing) and beta-amyloid (decreasing) are suitable marker for early AD diagnosis. The levels of tau protein and beta-amyloid in liquor were examined in a group of 21 patients with multiple sclerosis. Additionally, in patients with dementia genotyping of apolipoprotein E was carried out and the biochemical and genetic results of the measurements were compared with clinical findings. Tau protein levels in liquor were increased in 67 % of patients with AD, in 7 % in patients with vascular dementia (VD) and 17% in patients with mixed dementia (MD). Beta-amyloid levels were decreased in 67 % od AD, 33 % of VD and 33 % of MD. Contemporary tau protein increasing and beta-amyloid decreasing was find in 50 % of AD, 22 % of VD and 0 % od MD. In control set of patients with multiple sclerosis tau protein levels were increased in any case (in opposite level was decreased in 71 %); beta-amyloid decreasing was in 81 % cases. On base evaluating of tau protein and beta-amyloid proportions was possible confirm clinical diagnosis of AD surely in 50 % cases, bordeline in 33 % cases. 1. Hulstaert F, Blennow K, Ivanoiu A et al. Improved discrimination of AD patients using beta-amyloid(1-42) and tau levels in CSF. Neurology 1999; 52(8):1533-4. 2. Andreasen N, Minthon L, Davidsson P et al. Evaluation of CSF-tau and CSF-Abeta42 as diagnostic markers for Alzheimer disease in clinical practice. Arch Neurol 2001; 58:349-50.H
NR19 Predictors of Eating Disorder: Symptoms Across Ethnic Groups
Marney A. White, Ph.D., Psychiatry Department, Yale University, 301 Cedar Street, Second Floor, New Haven, CT 06519; Carlos M. Grilo, Ph.D.
At the conclusion of this session, the participant should be able to understand different components of eating and body image disturbances in adolescent girls and understand the predictors of these symptoms across ethnic groups.
Objective: To examine ethnicity patterns in eating and body image disturbances in psychiatrically hospitalized female adolescents.
Method: Subjects were 427 (54 African American, 320 Caucasian, 53 Latina) inpatients. Ethnic groups were compared on measures of dietary restraint, body image, binge eating, and purging. Psychological measures (depression, anxiety, impulsivity, self-devaluation, peer insecurity, child abuse) were examined as predictors of these eating and body image disturbances separately for the ethnic groups.
Results: Caucasians reported significantly higher levels of body image disturbance and dietary restraint than African Americans and Latinas (p < .001); binge eating and purging did not differ by ethnicity. Regression analyses indicated that for Caucasian and Latina girls, body image (43.8%, 47.1% of the variance) was explained by self-devaluation. For African Americans, body image (63% of the variance) was explained by self-devaluation, peer insecurity, and anxiety. For Caucasians, dietary restraint (34.8% of the variance) was explained by body image, depression, peer insecurity, and child abuse. For Latinas, restraint (32.9% of the variance) was explained by body image and impulsivity, whereas for African American girls, only body image disturbance predicted restraint (29.7% of the variance).
Conclusions: These findings indicate that different factors may contribute to the development of eating and body image psychopathology across ethnic groups. Findings raise questions regarding aspects of existing models of eating disorders for minority girls. 1. Barry DT, Grilo CM. Eating and body image disturbances in adolescent psychiatric inpatients: gender and ethnicity patterns. Int J Eat Disord 32: 335-343, 2002. 2. White MA, Kohlmaier JR, Varnado-Sullivan P, Williamson DA. Racial/ethnic differences in weight concerns: protective and risk factors for the development of eating disorders and obesity among adolescent females. Eating Weight Disord 8:20-25, 2003.
NR20 Body Dissatisfaction After Weight Restoration in Anorexia Nervosa
Joanna E. Steinglass, M.D., Department of Psychiatry, New York State Psychiatric Institute, 1051 Riverside Drive, Unit 98, New York, NY 10032; Laurel Mayer, M.D., B. Timothy Walsh, M.D.
At the conclusion of this session, the participant should be able to recognize the complexity of body image disturbance in anorexia nervosa and appreciate that the course of psychological improvement may be distinct from physical improvement.
Objective: This study aimed to assess change in body image in women with anorexia nervosa (AN) by assessing body dissatisfaction (BD) with weight normalization, as compared to controls.
Method: Subjects were 17 women hospitalized for AN, and 7 normal controls. BD was measured before and after weight gain and after 6 months of weight maintenance, using the Eating Disorder Inventory-Body Dissatisfaction subscale (EDI-BD) and the Color-A-Person Test (CAPT). The CAPT provides a measure of the affective component of body image. Subjects also completed standard psychological measures.
Results: At low weight, patients had significantly higher scores on both measures of BD compared to controls. After weight restoration, there was no significant change in BD scores, despite significant improvement in depression and anxiety. Data collection is ongoing, but preliminary analysis of the follow-up data (N=5) shows significant improvement on the CAPT.
Conclusions: BD neither worsens nor improves with weight normalization in hospitalized women undergoing treatment for AN. There may be significant improvement in BD with weight maintenance. 1. Cash T, Deagle, E: The nature and extent of body-image disturbances in anorexia nervosa and bulimia nervosa: a meta-analysis. Int J Eat Disord 1989; 8:499-509 2. Probst M, Vandereycken W, Van Coppenolle H, Pieters G: Body experience in eating disorders before and after treatment: a follow up study. European Psychiatry 1999; 14:333-340
NR21 Appearance Versus Health Reasons Among Obese Patients With Binge-Eating Disorder
Deborah L. Reas, Ph.D., Psychiatry Department, Yale School of Medicine, 301 Cedar Street, PO Box 208098, New Haven, CT 06520-8098; Carlos M. Grilo, Ph.D., Robin M. Masheb, Ph.D.
At the conclusion of this session, the participant should be able to understand the importance of assessing reasons for treatment seeking among obese patients with binge eating disorder and recognize the clinical implications of treatment seeking due to appearance concerns.
Objective: This study examined reasons for seeking treatment reported by obese men and women diagnosed with binge eating disorder (BED).
Method: Participants were 248 consecutive treatment-seeking obese adults (58 men and 190 women) who met DSM-IV criteria for BED, based on semi-structured diagnostic interviews. Patients’ reasons for seeking treatment were examined with respect to demography (gender and age), obesity (BMI and age of onset), features of eating disorders, and associated psychological functioning (depression and self-esteem).
Results: Of the 248 participants, 64% reported health concerns and 36% reported appearance concerns as their primary reason for seeking treatment. Reported reasons for seeking treatment did not differ significantly by gender. Patients seeking treatment due to appearance-related reasons had significantly lower BMIs than those reporting health-related reasons (BMI = 34.8 versus 38.5, respectively; p<001), but reported significantly greater body dissatisfaction (p<.001), significantly more features of eating disorders (p<.05), and lower self-esteem (p=.02).
Conclusions: Reasons that prompt treatment seeking among obese individuals with binge eating disorder warrant assessment and consideration during treatment planning, as they reflect meaningful patient characteristics. 1. Cheskin L, Donze LF. Appearance versus health as motivators for weight loss. J Am Med Assoc. 2001; 286:2160. 2. Levy A, Heaton A. Weight control practices of U.S. adults trying to lose weight. Annals Intern Med. 1993; 119(7S):661-666.
NR22 Clinic Bias in Binge-Eating Disorder Exists for Black Women
Christine Lozano-Blanco, Ph.D., Psychiatry Department, Yale School of Medicine, 301 Cedar Street, New Haven, CT 06519; Robin M. Masheb, Ph.D., Carlos M. Grilo, Ph.D.
At the conclusion of this session, the participant should be able to diagnose binge eating disorder and recognize differences in clinical characteristics of black and white women who seek or do not seek treatment.
Objective: To investigate sampling bias as it affects recruited clinic samples of black and white women with binge eating disorder (BED).
Methods: Clinical characteristics of a recruited clinic sample (220 consecutive BED cases) were compared with a community sample. Comparisons were performed separately for black and white women. Clinic and community groups were assessed with identical methods, including diagnostic interviews and established measures of features of eating disorders.
Results: In the clinic group, black and white women did not differ significantly in binge eating or eating-related psychopathology, but black women had significantly higher body mass index (BMI)(p < .001; effect size = .97). Among white women, the clinic and community samples did not differ significantly in BMI and had similar levels of eating-related psychopathology. Among black women, the clinic sample had significantly higher BMI (p < .005; effect size = .75), substantially higher eating-related psychopathology (effect sizes ranged .48 to 1.25), but reported lower frequencies of binge eating than the community sample (effect size = -.57).
Conclusions: Our findings suggest that there does not appear to be a sampling bias among recruited clinic samples of white women with BED. A sampling bias appears to exist among clinic samples of black women with BED. 1. Pike KM, Dohm FA, Striegel-Moore RH, Wilfley DE, Fairburn CG. A comparison of black and white women with binge eating disorder. Am J Psychiatry 2001; 158:1455-1460. 2. Wilfley DE, Pike KM, Dohm FA, Striegel-Moore RH, Fairburn CG. Bias in binge eating disorder: how representative are recruited clinic samples? J Consult Clin Psychol. 2001; 69:383-388.
NR23 A Controlled Comparison of Standard and Appetite-Focused Cognitive-Behavior Therapy for Binge-Eating Disorder
Supported by National Institutes of Health Katherine A. Elder, Ph.D., Psychiatry Department, Yale University, 245 N. Main Street, Apt. 4, Wallingford, CT 06492; Linda W. Craighead, Ph.D., Arnica L. Buckner, M.A., Heather M. Niemeier, M.A., Meredith A. Dung, M.A.
At the conclusion of this session, the participant should be able to: 1) understand the rationale and techniques used in an appetite-based CBT treatment of binge eating disorder; 2) identify the key differences between standard and appetite-focused CBT; and 3) understand the efficacy of both treatments used as early interventions in a college-aged population.
Objective: To compare the efficacy of two early intervention group treatments for binge eating disorder (BED): Cognitive-behavioral therapy (CBT) and a modified version of CBT, appetite-focused CBT (CBT-AF).
Method: Twenty overweight college-aged women with subclinical or recent-onset BED were assigned to one of the two conditions and participated in 10 weekly sessions. Outcome was assessed at 1 and 4 months posttreatment.
Results: Overall, participants in the CBT and the CBT-AF treatment groups demonstrated substantial, but not differential, improvement in eating disorder psychopathology and general psychiatric distress. Participants reported significant change in the following areas: decrease in number of objective binge episodes (p <.001, partial h2 = .53) and reduction in eating disorder symptomatology (on the EDE-Q, p <.001, partial h2 = .53), as well as improvement in body image, and decline in general psychopathology. These gains were evident at 1- and 4-months posttreatment.
Conclusions: The results support the efficacy of both CBT-based early interventions for BED, and demonstrate that such treatments can be successfully delivered in a brief group format. Appetite monitoring may be a viable alternative to monitoring food intake within CBT in a subclinical or recent-onset population with BED. 1. Craighead LW, & Allen H. (1995). Appetite awareness training: A cognitive behavioral intervention for binge eating. Cognitive and Behavioral Practice, 2, 249-270. 2. Wilfley DE, Welch RR, Stein RI, Spurrell EB, Cohen LR, Saelens BE, Dounchis JZ, Frank MA, Wiseman CV, Matt GE. (2002). A randomized comparison of group cognitive-behavioral therapy and group interpersonal psychotherapy for the treatment of overweight individuals with binge eating disorder. Archives of General Psychiatry, 59, 713-721.
NR24 Childhood Abuse and Cluster “B” Comorbidity in Bipolar Disorder
Jessica L. Garno, Ph.D., Department of Psychology, Long Island University, 6 Silvermine Drive, South Salem, NY 10590; Joseph F. Goldberg, M.D., Paul M. Ramirez, Ph.D., Barry A. Ritzler, Ph.D.
At the conclusion of this session, the participant should be able to familiarize participants with the phenomenology, prevalence, and clinical impact of childhood abuse, personality disorder comorbidity and their correlates in patients with bipolar disorder.
Background: Phenomenologic overlap between bipolar disorder and borderline personality disorder has engendered ongoing debate about their nosologic distinctions and respective treatment outcomes. Childhood trauma has been implicated in the pathogenesis and self-destructive behaviors of borderline personality disorder, but less empirical study has addressed these features in bipolar illness, or their prevalence when both disorders co-occur.
Method: One hundred DSM-IV bipolar I and II patents underwent SCID I and II diagnoses to ascertain comorbid cluster “B” personality features. Lifetime suicide attempts, substance abuse, and related components of course and outcome were examined relative to Axis II comorbidity and childhood abuse.
Results: Thirty percent of bipolar subjects met DSM-IV criteria for cluster “B” personality disorders, which in turn were linked with histories of childhood emotional or physical abuse and emotional neglect, as well as more extensive substance abuse and lifetime suicide attempts. Logistic regression analysis indicated that suicide attempt histories were significantly associated with the presence of a cluster “B” co-diagnosis while controlling for childhood abuse histories, comorbid substance abuse, or current levels of depression.
Conclusions: Cluster “B” personality disorders complicate illness course in about one-third of DSM-IV bipolar patients, making an independent contribution to increased lifetime suicide risk. 1. Leverich GS, McElroy SL, Suppes T, et al. Early physical and sexual abuse associated with an adverse course of bipolar disorder. Biol Psychiatry 2002; 51:288-297. 2. Bolton S, Gunderson JG. Distinguishing borderline personality disorder from bipolar disorder: differential diagnosis and implications. Am J Psychiatry 1996; 153:1202-1207.
NR25 Do Antidepressants Improve Remission in Patients With Bipolar Disorder?
Tamara B. Pardo, B.A., Psychiatry Department, Cambridge Hospital, 1493 Cambridge Street, Cambridge, MA 02139; S. Nassir Ghaemi, M.D., Rif S. El-Mallakh, M.D., Claudia F. Baldassano, M.D., Michael J. Ostacher, M.D., Frederick K. Goodwin, M.D., Ross J. Baldessarini, M.D.
At the conclusion of this session, the participant should be able to understand the long-term effects of antidepressant use in bipolar disorder.
Objective: Chronic subsyndromal depression is the major morbidity of bipolar disorder (1). The long-term utility of antidepressants (AD) in reducing chronic depressive morbidity in bipolar disorder is not known (2). We report interim data from the first randomized study with modern antidepressants on this question.
Method: An interim analysis was conducted at halfway point of a 5-year study (n=33). Subjects first recovered from a major depressive episode for 2 months (on mood stabilizer plus antidepressant), then were openly randomized to either continue (n=14) or discontinue (n=19) AD (up to 1 year follow-up presented). Remission was defined as <2 DSM-IV mood criteria within the week prior to the visit (using methods of the Systematic Treatment Enhancement Program for Bipolar Disorder study, STEP-BD).
Results: Time in remission was similar in the AD discontinuation (74.2% of first year follow-up) versus continuation (67.3%) groups, after adjustment for potential confounders (rapid cycling, gender, substance abuse, psychosis, and antidepressant attitude) (b=2.20, 95% CI [-23.2, 27.6]).
Conclusions: These interim data suggest that AD continuation does not lead to increased time in remission in bipolar disorder, compared to AD discontinuation. 1. Judd LL, Akiskal HS, Schettler PJ, Endicott J, Maser J, Solomon DA, Leon AC, Rice JA, Keller MB: The long-term natural history of the weekly symptomatic status of bipolar I disorder. Arch Gen Psychiatry 2002; 59(6):530-7 2. Ghaemi SN, Ko JY, Goodwin FK: “Cade’s disease” and beyond: misdiagnosis, antidepressant use, and a proposed definition for bipolar spectrum disorder. Can J Psychiatry 2002; 47(2):125-34.
NR26 Antidepressant Discontinuation and Mood Episode Relapse in Bipolar Disorder
Douglas J. Hsu, B.S., Department of Psychiatry, Cambridge Hospital, 1493 Cambridge Street, Cambridge, MA 02139; S. Nassir Ghaemi, M.D., Rif S. El-Mallakh, M.D., Claudia F. Baldassano, M.D., Michael J. Ostacher, M.D., Frederick K. Goodwin, M.D., Ross J. Baldessarini, M.D.
At the conclusion of this session, the participant should be able to determine if antidepressant discontinuation leads to increased risk of relapse in bipolar disorder.
Objective: In a recent observational study, antidepressant continuation (using modern antidepressants) delayed relapse versus antidepressant discontinuation following recovery from bipolar depression (1). The only previous randomized study, conducted with TCAs, found no increased relapse with antidepressant discontinuation (2). We report interim data from the first randomized study with modern antidepressants on this question.
Method: An interim analysis was conducted at halfway point of a 5-year study (n=33). Subjects first recovered from a major depressive episode for 2 months (on mood stabilizer plus antidepressant), then were openly randomized to either continue (LT; n=14) or discontinue (ST; n=19) antidepressants (up to 1 year follow-up presented).
Results: In an unadjusted survival analysis of time to first mood episode, there was nonsignificant benefit in the LT group versus the ST group (HR=1.59±0.81, 95% CI [0.58, 4.31]). After adjusting for confounders (rapid cycling, gender, attitude towards antidepressants), there were no notable differences in the two groups (HR=1.21±0.73, 95% CI [0.37, 3.97]).
Conclusions: Observational evidence of increased risk of rapid depressive relapse with antidepressant discontinuation in bipolar disorder is likely liable to confounding factors. Randomization and adjustment for confounders suggests little evidence of increased risk of depressive relapse with antidepressant discontinuation, even with modern antidepressants. 1. Altshuler L, Suppes T, Black D, Nolen WA, Keck PE, Jr., Frye MA, McElroy S, Kupka R, Grunze H, Walden J, Leverich G, Denicoff K, Luckenbaugh D, Post R: Impact of antidepressant discontinuation after acute bipolar depression remission on rates of depressive relapse at 1-year follow-up. Am J Psychiatry 2003; 160(7):1252-62 2. Prien RF, Kupfer DJ, Mansky PA, Small JG, Tuason VB, Voss CB, Johnson WE: Drug therapy in the prevention of recurrences in unipolar and bipolar affective disorders: A report of the NIMH Collaborative Study Group comparing lithium carbonate, imipramine, and a lithium carbonate-imipramine combination. Arch Gen Psychiatry 1984; 41:1096-1104.
NR27 Risk for Recurrent Depression During the Postpartum Period: A Prospective Study
Ruta M. Nonacs, M.D., Department of Psychiatry, Massachusetts General Hospital, 15 Parkman Street, WACC 815, Boston, MA 02114; Lee S. Cohen, M.D., Adele C. Viguera, M.D., Alison Reminick, B.A., Bernard L. Harlow, Ph.D.
At the conclusion of this session, the participant should be able to recognize clinical and demographic variables that put women with recurrent major depression at risk for postpartum depression.
Background: The postpartum period is a time of heightened risk for psychiatric illness, particularly in women who have histories of depression. Given the prevalence of depressive disorders during the childbearing years and the negative effect of maternal depression on child development, it is crucial to identify those women at highest risk for depression during the postpartum period.
Methods: The authors prospectively followed 47 women with histories of pre-gravid DSM-IV major depression across pregnancy and into the postpartum period. Predictors of puerperal mood disturbance, including demographic and clinical variables, were examined.
Results: 48.9% of the women experienced a major depressive episode within three months following delivery. Higher rates of postpartum depression were observed in women with histories of postpartum depression and greater number of previous depressive episodes; however, these findings were not statistically significant. Women who experienced a recurrence of depression during pregnancy were at greatest risk for postpartum depression, particularly when the episode occurred proximate to delivery.
Conclusions: Women with histories of pre-gravid major depression are at high risk for relapse during the postpartum period, particularly if they experience depression during pregnancy. This population may be candidates for prophylactic interventions which may attenuate the risk of postpartum psychiatric illness. 1. Nonacs RM, Cohen LS. Postpartum mood disorders: Diagnosis and treatment guidelines. J Clin Psychiatry 59 (suppl 2): 34-30, 1998. 2. O’Hara MW, Schlechte JA, Lewis DA, Varner MW. Controlled prospective study of postpartum mood disorders: psychological, environmental, and hormonal factors. J Abnorm Psychol 100 (1): 63-73, 1991.
NR28 Treating Subsyndromal Symptoms to Prevent Affective Relapse
Calvin K. Yang, Psychiatry Department, University of Pennsylvania, 226 W. Rittenhouse Square, 604, Philadelphia, PA 19103; Claudia F. Baldassano, M.D., Mohit P. Chopra, M.D., Laszlo Gyulai, M.D.
At the conclusion of this session, the participant should be able to evaluate the hypothesis that the pharmacologic treatment of subsyndromal symptoms in patients with bipolar I or II disorder may prevent major affective relapse. Introduction: Studies have shown that both subsyndromal mania and subsyndromal depression in patients with bipolar I are predictive of major affective relapse with subsyndromal mania being more predictive of relapse than subsyndromal depression. However, no studies to date have investigated whether the pharmacologic treatment of subsyndromal symptoms can prevent affective relapse in patients with bipolar disorder. This study evaluates the protective effects of pharmacologically treating subsyndromal symptoms in bipolar patients.
Methods: A database of 75 episodes of subsyndromal episodes will be included in the analysis. Subsyndromal episodes were defined by STEP-BD (Systematic Treatment Enhancement Program for Bipolar Disorder) protocol as the occurrence of ³ 3 moderate symptoms that do not meet DSM-IV criteria for manic, mixed, or depressive episodes following a period of at least 8 consecutive weeks with no more than 2 moderate symptoms. With each subsyndromal episode, medication changes were recorded. Patients were evaluated for affective relapse using DSM-IV criteria.
Results: To date, a database of 163 patients has been systematically examined and 41 subsyndromal episodes with follow-up were identified across 29 patients. The sample included 13 men and 16 women, 26 bipolar type I and 3 bipolar type II. Analysis showed that 10/11 untreated subsyndromal episodes resulted in recovery while 22/30 treated subsyndromal episodes resulted in recovery. No significant difference was found in relapse rate between treated and untreated patients (Pearson Chi-Square, p=.234, df=1).
Conclusion: Treating subsyndromal manic, depressive, or mixed episodes may not protect against affective relapse in bipolar disorder. 1. Keller MB, Lavori PW, Kane, JM, et al. Subsyndromal symptoms in bipolar disorder: a comparison of standard and low serum levels of lithium. Archives of General Psychiatry 1992; 49:371-376. 2. Tohen M, Waternaux CM, Tsuang MT. Outcome in mania: a 4-year prospective follow-up of 75 patients utilizing survival analysis. Archives of General Psychiatry 1990; 47:1106-1111.
NR29 Risk Factors for Insulin Resistance and Depression: Analysis of NHANES I
James E. Gangwisch, Ph.D., Public Health Department, Columbia University, 614 West 114th Street, New York, NY 10025
From this session, the participant should be able to recognize the bidirectional relationship between insulin resistance and depression with depressed individuals engaging in poor health practice behaviors and with insulin resistance contributing toward depression by impairing insulin’s ability to promote brain serotonin synthesis and to suppress the reuptake of norepinephrine. Introduction/Hypothesis: Many depressed individuals have been found to engage in behaviors that are known risk factors for insulin resistance (IR). Cortisol release from stress has also been shown to have deleterious effects upon both insulin sensitivity and mood. This study was conducted to see whether individuals who are likely to suffer from insulin resistance based upon engagement in poor health practice behaviors would be more likely to suffer from depression while controlling for stress.
Methods: Logistic regression was used to examine the relationship between depression and the likelihood of being IR (based upon measures of risk factors for IR: BMI, hours sleep per night, physical activity, sweets consumption, and alcohol consumption) while controlling for stress.
Results: Subjects likely to be IR were 45% more likely to be depressed (odds ratio = 1.45; 95% CI = 1.28 to 1.63; p = .0001) than subjects unlikely to be IR after controlling for stress. Conclusions/Discussion: Subjects likely to be IR have increased rates of depression, which is consistent with findings that individuals with diabetes and cardiovascular disease are at greater risk of depression. This relationship is likely to be bidirectional, with depressed individuals being more likely to engage in poor health practice behaviors and with IR contributing toward depressed mood by impairing insulin’s ability to promote brain serotonin synthesis and
I guess so. Must be why no one wants me. Relax you will get something.
hmm.i know with certain situations you have to wait, like 5 years i think.
Anxiety
Tips
Proper diet : This includes reduction in consumption of caffeine, sugar, and generally an improvement of eating habits. Caffeine reduction should be gradual. Some anxiety sufferers report considerable reductions in their anxiety just from taking these measures.
Exercise : Some exercise is thought to relieve stress. Anxiety sufferers should note that rapid heart palpitations during exercise can trigger a panic attack, so it is probably better to gradually develop an exercise routine while on a cognitive-behavioral program.
Laughing :
Breathing techniques and proper breathing : A diaphragmic breathing technique is often recommended (as opposed to chest breathing).
Proper sleep:
Relaxation techniques : A state of relaxation can be achieved with the help of relaxation tapes, Yoga or relaxation therapy.
Stress management : This may entail changes in lifestyle and time management. There are a number of books specialized in stress management.
Panic attack coping strategies : Specific strategies for dealing with panic episodes have been proposed, such as slow abdominal breathing and use of reassuring self-talk.
Search for meaning and purpose : Some experts have indicated that residual generalized anxiety can be the result of a sort of "boredom" about existence. They recommend looking for an occupation the sufferer finds meaningful.
Source(s):
www.wikipedia.com
yes they can, depends on the job position.when the counselor calls make sure they are aware that your condition is fixed.i work for the department of corrections and i take anxiety pills, in order to pass the full screening, i had to also talk to a counselor, they talked to me for about an hour, the next week i had the job.
Answers: