lederr

Archive for the ‘General Psychology’ Category

Adult ADHD And Women: Many Fall Through The Cracks!

In ADHD, ADHD Adult, General Psychology, Psychiatry on Sunday, 30 March 2014 at 04:30

http://www.adultadhdblog.com/2014/03/28/adult-adhd-and-women-2/

Phillip Seymour Hoffman did not have choice or free will and neither do you.

In ADHD, Anxiety, Brain imaging, Brain studies, Child/Adolescent Psychology, General Psychology, Medicine, Mood Disorders, Neuropsychology, Neuroscience, Psychiatry on Tuesday, 11 March 2014 at 12:37

one of the best things about this subject that i’ve read in a long time.  give it a read. it makes you think.

Phillip Seymour Hoffman did not have choice or free will and neither do you..

suicide is not painless…

In General Psychology, Psychiatry, School Psychology on Wednesday, 19 February 2014 at 17:30

http://mag.newsweek.com/2013/05/22/why-suicide-has-become-and-epidemic-and-what-we-can-do-to-help.html

Asperger Syndrome Revisited

In Autism Spectrum Disorders, General Psychology, Psychiatry, School Psychology, Special Education on Wednesday, 11 December 2013 at 05:59

Asperger Syndrome Revisited

By: Lee Wilkinson, Ph.D.

The deletion of Asperger’s disorder (Asperger’s syndrome) as a separate diagnostic category from the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) has been widely publicized. The new DSM-5 category of autism spectrum disorder (ASD), which subsumes the previous DSM-IV diagnoses of autistic disorder (autism), Asperger’s disorder, and pervasive developmental disorder not otherwise specified (PDD-NOS), reflects the scientific consensus that symptoms of the various DSM-IV subgroups represent a single continuum of impairment that varies in level of severity and need for support.

An important feature of the DSM-5 criteria for ASD is a change from three symptom domains (triad) of social impairment, communication deficits and repetitive/restricted behaviors, interests, or activities to two domains (dyad); social/communication deficits and fixated and repetitive pattern of behaviors. Several social/communication criteria were merged to clarify diagnostic requirements and reflect research indicating that language deficits are neither universal in ASD, nor should they be considered as a defining feature of the diagnosis. The criteria also feature dimensions of severity that include current levels of language and intellectual functioning as well as greater flexibility in the criteria for age of onset and addition of symptoms not previously included in the DSM-IV such as sensory interests and aversions.

DSM-IV Criteria in Practice

Problems in applying the DSM-IV criteria were a key consideration in the decision to delete Asperger’s disorder as a separate diagnostic entity. Numerous studies indicate that it is difficult to reliably distinguish between Asperger syndrome, autism, and other disorders on the spectrum in clinical practice (Attwood, 2006; Macintosh & Dissanayake, 2006; Leekam, Libby, Wing, Gould & Gillberg, 2000; Mayes & Calhoun, 2003; Mayes, Calhoun, & Crites, 2001; Miller & Ozonoff, 2000; Ozonoff, Dawson, & McPartland, 2002; Witwer & Lecavalier, 2008). For example, children with autism who develop proficient language have very similar trajectories and later outcomes as children with Asperger disorder (Bennett et al., 2008; Howlin, 2003; Szatmari et al., 2000) and the two are indistinguishable by school-age (Macintosh & Dissanayake, 2004), adolescence (Eisenmajer, Prior, Leekam, Wing, Ong, Gould & Welham 1998; Ozonoff, South and Miller 2000) and adulthood (Howlin, 2003). Individuals with Asperger disorder also typically meet the DSM-IV communication criterion of autism, “marked impairment in the ability to initiate or sustain a conversation with others,” making it is possible for someone who meets the criteria for Asperger’s disorder to also meet the criteria for autistic disorder.

Treatment and Outcome

Another important consideration was response to treatment. Intervention research cannot predict, at the present time, which particular intervention approach works best with which individual. Likewise, data is not available on the differential responsiveness of children with Asperger’s disorder and high-functioning autism to specific interventions (Carpenter, Soorya, & Halpern, 2009). There are no empirical studies demonstrating the need for different treatments or different responses to the same treatment, and in clinical practice the same interventions are typically offered for both autism and Asperger’s disorder (Wilkinson, 2010). Treatments for impairments in pragmatic (social) language and social skills are the same for both groups.

Application of the New Criteria

It’s important to remember that in the DSM, a mental disorder is conceptualized as a clinically important collection of behavioral and psychological symptoms that causes an individual distress, disability or impairment. The objective of new DSM-5 criteria for ASD is that every individual who has significant “impairment” in social-communication and restricted and repetitive behavior or interests should meet the diagnostic criteria for ASD.  Because language impairment/delay is not a necessary criterion for diagnosis, anyone who demonstrates severe and sustained impairments in social skills and restricted, repetitive patterns of behavior, interests, or activities in the presence of generally age-appropriate language acquisition and cognitive functioning, who might previously have been given a diagnosis of Asperger’s disorder, will now meet the criteria for ASD.

The new DSM-5 criteria for ASD have created significant controversy over concerns that it would exclude many individuals currently diagnosed with Asperger syndrome and PDD-NOS, and thus make it difficult for them to access services. However, recently published field trials suggest that the revisions actually increase the reliability of diagnosis, while identifying the large majority of those who would have been diagnosed under the DSM-IV-TR. Of the small numbers who were not included, most received the new diagnosis of “social communication disorder.” Moreover, the accuracy of non-spectrum classification (specificity) made by DSM-5 was better than that of DSM-IV, indicating greater effectiveness in distinguishing ASD from non-spectrum disorders such as language disorders, intellectual disability, attention-deficit/hyperactivity disorder (ADHD), and anxiety disorders. It is also important to note that all individuals who have a DSM-IV diagnosis on the autism spectrum, including those with Asperger syndrome and PDD-NOS, will be able to retain an ASD diagnosis. This means that no one should “lose” their diagnosis because of the changes in diagnostic criteria.  According to DSM-5, individuals with a well-established DSM-IV diagnosis of Autistic Disorder, Asperger’s Disorder, or PDD-NOS should be given a diagnosis of ASD.  Those who have marked deficits in social communication, but whose symptoms do not meet the criteria for ASD, should be evaluated for Social (Pragmatic) Communication Disorder.

Conclusion

In conclusion, the DSM-5 category of autism spectrum disorder (ASD), which subsumes the current diagnoses of autistic disorder, Asperger’s disorder, and pervasive developmental disorder not otherwise specified (PDD-NOS), better describes our current understanding about the clinical presentation and course of the neurodevelopmental disorders. Conceptualizing autism as a spectrum condition rather than a categorical diagnostic entity is in keeping with the extant research suggesting that there is no clear evidence that Asperger’s disorder and high-functioning autism are different disorders. As Gillberg (2001) notes, the terms Asperger’s syndrome and high-functioning autism are more likely “synonyms” than labels for different disorders. Lord (2011) also comments that although there has been much controversy about whether there should be separate diagnoses, “Most of the research has suggested that Asperger’s syndrome really isn’t different from other autism spectrum disorders.” “The take-home message is that there really should be just a general category of autism spectrum disorder, and then clinicians should be able to describe a child’s severity on these separate dimensions.” Unfortunately, many individuals may have been advised (or assumed) that a diagnosis of Asperger’s disorder was separate and distinct from autistic disorder and that intervention/treatment, course, and outcome were clinically different for each disorder. While including Asperger’s Disorder under the DSM-5 category of ASD will likely continue to require a period of transition and adjustment, the proposed dimensional approach to diagnosis will likely result in more effective identification, treatment, and research for individuals on the spectrum.

References

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders. Washington, DC: Author.

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders(4th ed., text rev.). Washington, DC: Author.

American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders(5th ed.). Washington, DC: Author.

Attwood, T. (2006). The complete guide to Asperger’s syndrome. London: Jessica Kingsley.

Carpenter, L. A., Soorya, L. & Halpern, D. (2009). Asperger’s syndrome and high- functioning autism. Pediatric Annals, 38, 30-35.

Eisenmajer, R., Prior, M., Leekam, S., Wing, L., Ong, B., Gould, J. & Welham, M. (1998)

Delayed Language Onset as a Predictor of Clinical Symptoms in Pervasive Developmental Disorders. Journal of Autism and Developmental Disorders, 28, 527–34.

Gillberg, C (2001). Asperger’s syndrome and high functioning autism: Shared deficits or

different Disorders? Journal of Developmental and Learning Disorders, 5, 79-94.

Howlin, P. (2003). Outcome in high-functioning adults with autism with and without early language delays: Implications for the differentiation between autism and Asperger syndrome. Journal of Autism and Developmental Disorders, 33, 3–13.

Leekam, S., Libby, S., Wing, L., Gould, J. & Gillberg, C. (2000) Comparison of ICD-10 and Gillberg’s criteria for Asperger syndrome. Autism, 4, 11–28.

Lord, C. et al. (2011). A multisite study of the clinical diagnosis of different autism spectrum disorders. Archives of General Psychiatry. doi:10.1001/archgenpsychiatry.2011.148

Macintosh, K., & Dissanayake, C. (2006). Social skills and problem behaviors in school aged children with high-functioning autism and Asperger’s disorder. Journal of Autism and Developmental Disorders, 36, 1065–1076.

Macintosh, K.E., & Dissanayake, C. (2004). Annotation: The similarities and differences

between autistic disorder and Asperger’s disorder: A review of the empirical evidence. Journal of Child Psychology and Psychiatry, 45, 421–434.

Mayes, S., & Calhoun, S. (2003). Relationship between Asperger syndrome and high functioning autism. In M. Prior (Ed.), Learning and behavior problems in Asperger syndrome (pp. 15-34). New York: Guilford Press.

Mayes SD, Calhoun SL, Crites DL (2001) Does DSM-IV Asperger’s disorder exist? Journal of Abnormal Child Psychology, 29, 263–271.

Miller, J. N., & Ozonoff, S. (2000). The external validity of Asperger disorder: Lack of evidence from the domain of neuropsychology. Journal of Abnormal Psychology, 109, 227–238.

Ozonoff, S., Dawson, G., & McPartland, J. (2002). A parent’s guide to Asperger syndrome and high-functioning autism: How to meet the challenges and help your child to thrive. New York: Guilford Press.

Ozonoff, S., South, M., & Miller, J. N. (2000). DSM-IV-defined Asperger syndrome: Cognitive, behavioral and early history differentiation from high-functioning autism. Autism, 4, 29–46.

Szatmari, P., Bryson, S.E., Streiner, D.L., Wilson, F.J., Archer, L., & Ryerse, C. (2000). Two year outcome of preschool children with autism or Asperger’s syndrome. American Journal of Psychiatry, 15, 1980–1987.

Szatmari, P., Bryson, S., Duku, E., Vaccarella, L., Zwaigenbaum, L., Bennett, L. & Boyle, M.H. (2009). Similar developmental trajectories in autism and Asperger syndrome: from early childhood to adolescence. Journal of Child Psychology and Psychiatry, 50, 1459-1467.

Wilkinson, L. A. (2008). Adults with Asperger syndrome: A childhood disorder grows up. The Psychologist, 21, 764-770.

Wilkinson, L. A. (2010). A best practice guide to assessment and intervention for Asperger syndrome and autism in schools. London: Jessica Kingsley Publishers.

Wilkinson, L. A. (Ed.) (in press). Autism spectrum disorder in children and adolescents: Evidence-based assessment and intervention in schools. American Psychological Association (APA): Washington, DC.

Williams, K., Tuck, M., Helmer, M., Bartak, L., Mellis, C. & Peat, J.K. (2008). Diagnostic labelling of autism spectrum disorders in NSW. Journal of Paediatrics and Child Health, 44, 108-113.

Wing, L. (2005). Problems of categorical classification systems. In F. R. Volkmar, R. Paul, A. Klin, & D. Cohen (Eds.),Handbook of autism and pervasive developmental disorders: Vol. 1. Diagnosis, development, neurobiology, and behavior (3rd ed., pp. 583–605). New York: John Wiley.

Witwer, A.N., & Lecavalier, L. (2008). Validity of autism spectrum disorder subtypes. Journal of Autism and Developmental Disorders, 38, 1611–1624.

Lee A. Wilkinson, PhD, CCBT, NCSP is author of the award-winning book, A Best Practice Guide to Assessment and Intervention for Autism and Asperger Syndrome in Schools, published by Jessica Kingsley Publishers.

Retrieved from: http://bestpracticeautism.blogspot.com/2013/12/asperger-syndrome-revisited.html?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+BestPracticeAutism+%28Best+Practice+Autism%29

 

weed…it’s not just for breakfast anymore…

In Alternative Health, General Psychology, Medication, Medicine on Wednesday, 21 August 2013 at 08:21

i have always respected sanjay gupta and appreciate that he, unlike MANY others in medicine and related fields, is able to apologize and say he was wrong and has researched the topic and come up with his professional opinions based on data and experience. we put so many legal drugs into our systems with serious side effects but think nothing of it since they are prescribed by doctors. perhaps it is time to look at alternative medicine. especially that that is natural and not chemically manufactured. how many times do we hear about drugs recalls based on serious side effects (including death) that have been prescribed or the misuse and abuse of “legal” drugs. we have bigger problems than “weed.” as for recreational drugs, alcohol kills from accidents, abuse, overdose, etc., but there are no discussions to go back to prohibition. very interesting article.

http://www.cnn.com/2013/08/08/health/gupta-changed-mind-marijuana/index.html?sr=sharebar_facebook

what they eyes say about adhd…

In ADHD, ADHD Adult, ADHD child/adolescent, Child/Adolescent Psychology, General Psychology, Neuropsychology, Psychiatry on Tuesday, 21 May 2013 at 06:51

Eye May Be Key to More Accurate ADHD Diagnosis

Megan Brooks

SAN FRANCISCO — Examining the retina may aid in the diagnosis of attention-deficit/hyperactivity disorder (ADHD), new research suggests.

A small study by investigators at Albert-Ludwigs University of Freiburg, Germany, showed that patients with ADHD displayed significantly elevated “background noise” on a pattern electroretinogram (PERG) compared with their healthy peers.

Altered visual signal processing may be a “neuronal correlate for ADHD,” study presenter Emanuel Bubl, MD, told Medscape Medical News. “If we can replicate this finding, it would be of great clinical importance because it would be an objective marker of ADHD.”

Dr. Bubl presented the study here at the American Psychiatric Association’s 2013 Annual Meeting.

PERG — which is a kin to an electrocardiogram of the retina — provides an electrophysiologic measurement of the activity of the retinal ganglion cells.

“This technique is an easy-to-apply and already well-established instrument in ophthalmology. With adaption, it could be widely used,” Dr. Bubl said.

Inattention and distractability are core symptoms of ADHD, but a “clearcut neuronal correlate is missing. Any attempt to find objective markers of ADHD would be very helpful in this context,” Dr. Bubl said.

Dr. Bubl and colleagues used PERG to measure the response of the retina to a checkerboard visual stimuli in 20 patients with ADHD and 20 healthy control participants.

“An elevated neuronal noise or background firing has been proposed as an underlining pathophysiological mechanism and treatment target. We found evidence for an early alteration in visual perception or signal transmission in patients with ADHD, with significantly elevated neuronal noise (P < .014),” said Dr. Bubl. In particular, neuronal noise significantly correlated with inattention, as measured with the Conners’ Adult ADHD Rating Scale.

“The results might explain why patients with ADHD are easily distracted,” Dr. Bubl added.

With more study, the results could have potentially important clinical implications. “With ADHD, there is a debate about the existence of the disease on the one hand and a growing concern about overdiagnosing ADHD and prescription of medication on the other,” he said.

With PERG, the diagnosis of ADHD could be “objectified by measurable signals, and this would be dramatically helpful in the controversial public discussion.” Use of PERG might also help in determining the effects of methylphenidate or psychotherapy on ADHD.

The authors report no relevant financial relationships.

The American Psychiatric Association’s 2013 Annual Meeting. Abstract SCR02-2. Presented May 18, 2013.

Retrieved from: http://www.medscape.com/viewarticle/804409?src=nl_topic&uac=184795PG

NIMH abandoning DSM V

In General Psychology, Neuropsychology, Psychiatry on Wednesday, 8 May 2013 at 08:03

National Institute of Mental Health abandoning the DSM

In a potentially seismic move, the National Institute of Mental Health – the world’s biggest mental health research funder, has announced only two weeks before the launch of the DSM-5diagnostic manual that it will be “re-orienting its research away from DSM categories”.

In the announcement, NIMH Director Thomas Insel says the DSM lacks validity and that “patients with mental disorders deserve better”.

This is something that will make very uncomfortable reading for the American Psychiatric Association as they trumpet what they claim is the ‘future of psychiatric diagnosis’ only two weeks before it hits the shelves.

As a result the NIMH will now be preferentially funding research that does not stick to DSM categories:

Going forward, we will be supporting research projects that look across current categories – or sub-divide current categories – to begin to develop a better system. What does this mean for applicants? Clinical trials might study all patients in a mood clinic rather than those meeting strict major depressive disorder criteria. Studies of biomarkers for “depression” might begin by looking across many disorders with anhedonia or emotional appraisal bias or psychomotor retardation to understand the circuitry underlying these symptoms. What does this mean for patients? We are committed to new and better treatments, but we feel this will only happen by developing a more precise diagnostic system.

As an alternative approach, Insel suggests the Research Domain Criteria (RDoC) project, which aims to uncover what it sees as the ‘component parts’ of psychological dysregulation by understanding difficulties in terms of cognitive, neural and genetic differences.

For example, difficulties with regulating the arousal system might be equally as involved in generating anxiety in PTSD as generating manic states in bipolar disorder.

Of course, this ‘component part’ approach is already a large part of mental health research but the RDoC project aims to combine this into a system that allows these to be mapped out and integrated.

It’s worth saying that this won’t be changing how psychiatrists treat their patients any time soon. DSM-style disorders will still be the order of the day, not least because a great deal of the evidence for the effectiveness of medication is based on giving people standard diagnoses.

It is also true to say that RDoC is currently little more than a plan at the moment – a bit like the Mars mission: you can see how it would be feasible but actually getting there seems a long way off. In fact, until now, the RDoC project has largely been considered to be an experimental project in thinking up alternative approaches.

The project was partly thought to be radical because it has many similarities to the approach taken by scientific critics of mainstream psychiatry who have argued for a symptom-based approach to understanding mental health difficulties that has often been rejected by the ‘diagnoses represent distinct diseases’ camp.

The NIMH has often been one of the most staunch supporters of the latter view, so the fact that it has put the RDoC front and centre is not only a slap in the face for the American Psychiatric Association and the DSM, it also heralds a massive change in how we might think of mental disorders in decades to come.

Link to NIMH announcement ‘Transforming Diagnosis’.

Retrieved from: http://mindhacks.com/2013/05/03/national-institute-of-mental-health-abandoning-the-dsm/

transforming diagnosis

In Brain imaging, General Psychology, Neuropsychology, Psychiatry on Wednesday, 8 May 2013 at 07:58

http://www.nimh.nih.gov/about/director/2013/transforming-diagnosis.shtml.

a visual guide to happiness and others…love this!

In General Psychology, Happiness, Mindfulness on Saturday, 30 March 2013 at 04:25

http://staroversky.com/visual-guide-to-happiness/?goback=%2Egde_58284_member_225378601

genes, genes…

In ADHD, ADHD Adult, ADHD child/adolescent, Autism Spectrum Disorders, General Psychology, Genes, Neuropsychology, Neuroscience, Personality Disorders, Psychiatry on Friday, 1 March 2013 at 06:15

i love gwas and really feel it will continue to broaden our understanding of psychiatric illnesses and, hopefully, lead to better treatment options.

Five Major Psychiatric Disorders Genetically Linked

By: Caroline Cassels

In the largest genetic study of psychiatric illness to date, scientists have discovered genetic links between 5 major psychiatric disorders.

Investigators from the Cross-Disorder Group of the Psychiatric Genomics Consortium have found that autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BD), major depressive disorder (MDD), and schizophrenia share common genetic risk factors.

Specifically, the results of the genome-wide association study (GWAS) reveal single-nucleotide polymorphisms (SNPs) in 2 genes —CACNA1C and CACNB2 — both of which are involved in the balance of calcium in brain cells, are implicated in several of these disorders, and could provide a potential target for new treatments.

“This analysis provides the first genome-wide evidence that individual and aggregate molecular genetic risk factors are shared between 5 childhood-onset or adult-onset psychiatric disorders that are treated as distinct categories in clinical practice,” study investigator Jordan Smoller, MD, Massachusetts General Hospital, Boston, said in a release.

The study was published online February 28 in the Lancet.

Potential Therapeutic Target

The researchers note that findings from family and twin studies suggest that genetic risks for psychiatric disorders do not always map to current diagnostic categories and that “doubt remains about the boundaries between the syndromes and the disorders that have overlapping foundations or different variants of one underlying disease.”

“The pathogenic mechanisms of psychiatric disorders are largely unknown, so diagnostic boundaries are difficult to define. Genetic risk factors are important in the causation of all major psychiatric disorders, and genetic strategies are widely used to assess potential overlaps,” the investigators write.

The aim of the study was to identify specific variants underlying genetic effects shared between 5 major psychiatric disorders: ASD, ADHD, BD, MDD, and schizophrenia.

The researchers analyzed genome-wide SNP data for the 5 disorders in 33,332 cases and 27,888 control participants of European ancestry. They identified 4 risk loci that have significant and overlapping links with all 5 diseases. These included regions on chromosomes 3p21 and 10q24, and SNPs in the gene CACNA1C,which has previously been linked to bipolar disorder and schizophrenia, and in theCACNB2 gene.

Polygenic risk scores confirmed cross-disorder effects, most strongly between adult-onset disorders BD and MDD and schizophrenia. Further pathway analysis corroborated that calcium channel activity could play an important role in the development of all 5 disorders.

“Significant progress has been made in understanding the genetic risk factors underlying psychiatric disorders. Our results provide new evidence that may inform a move beyond descriptive syndromes in psychiatry and towards classification based on underlying causes.

“These findings are particularly relevant in view of the imminent revision of classifications in the Diagnostic and Statistical Manual of Mental Disorders and the International Classification of Diseases,” said Dr. Smoller.

The investigators add that the study results “implicate a specific biological pathway — voltage-gated calcium-channel signalling — as a contributor to the pathogenesis of several psychiatric disorders, and support the potential of this pathway as a therapeutic target for psychiatric disease.”

In an accompanying editorial, Alessandro Serretti, MD, PhD, and Chiara Fabbri, MD, from the University of Bologna, Italy, assert that “the main innovative contribution of the present study is the combination of qualitative and quantitative analyses of the shared genetic features associated with vulnerability of these 5 disorders.”

They add, “the present study might contribute to future nosographic systems, which could be based not only on statistically determined clinical categories, but also on biological pathogenic factors that are pivotal to the identification of suitable treatments.”

The authors and editorialists have reported no relevant financial relationships.

Retrieved from: http://www.medscape.com/viewarticle/779979?src=nl_topic

Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis

Background

Findings from family and twin studies suggest that genetic contributions to psychiatric disorders do not in all cases map to present diagnostic categories. We aimed to identify specific variants underlying genetic effects shared between the five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia.

Methods

We analysed genome-wide single-nucleotide polymorphism (SNP) data for the five disorders in 33 332 cases and 27 888 controls of European ancestory. To characterise allelic effects on each disorder, we applied a multinomial logistic regression procedure with model selection to identify the best-fitting model of relations between genotype and phenotype. We examined cross-disorder effects of genome-wide significant loci previously identified for bipolar disorder and schizophrenia, and used polygenic risk-score analysis to examine such effects from a broader set of common variants. We undertook pathway analyses to establish the biological associations underlying genetic overlap for the five disorders. We used enrichment analysis of expression quantitative trait loci (eQTL) data to assess whether SNPs with cross-disorder association were enriched for regulatory SNPs in post-mortem brain-tissue samples.

Findings

SNPs at four loci surpassed the cutoff for genome-wide significance (p<5×10−8) in the primary analysis: regions on chromosomes 3p21 and 10q24, and SNPs within two L-type voltage-gated calcium channel subunits, CACNA1C and CACNB2. Model selection analysis supported effects of these loci for several disorders. Loci previously associated with bipolar disorder or schizophrenia had variable diagnostic specificity. Polygenic risk scores showed cross-disorder associations, notably between adult-onset disorders. Pathway analysis supported a role for calcium channel signalling genes for all five disorders. Finally, SNPs with evidence of cross-disorder association were enriched for brain eQTL markers.

Interpretation

Our findings show that specific SNPs are associated with a range of psychiatric disorders of childhood onset or adult onset. In particular, variation in calcium-channel activity genes seems to have pleiotropic effects on psychopathology. These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.

Funding-National Institute of Mental Health.

Retrieved from: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)62129-1/abstract

Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis
Cross-Disorder Group of the Psychiatric Genomics Consortium
The Lancet – 28 February 2013
DOI: 10.1016/S0140-6736(12)62129-1

bye bye, bipolar disorder!

In Education, General Psychology, Mood Disorders, School Psychology on Tuesday, 19 February 2013 at 06:57

i love this website and the information.  i find it useful in general and in my work in the schools.  if you work with children with behavioral issues or are interested in learning more, i recommend you join dr. mac’s b-list email list.  i always find interesting and useful articles like the one below.  thanks, dr, mac!

Bye-Bye Bi-Polar Disorder

Hello again, fellow B-Lister!  Where are you located right now on the mood spectrum?  Forlorn?  So-So?  Ecstatic?  How’s the energy level right now? Are you sinking into the sofa for the 3rd day in a row, taking a short-lived seat to read this communication, or jumping up and down on it?

We all have ups and downs in mood, energy, or ability to function well in our daily tasks.  Some folks, though,  re-cycle through these ups and downs, reaching the extreme ends of the continuum.

Back-in-the-day, I typically heard the term “Manic Depression” used for the condition under discussion in our newsletter today.  When I first heard the term “Bi-Polar”, I thought it had something to do with the melting of the polar ice caps or penguins moving up to Santa’s domain!

Bipolar disorder: A mental illness that is evidenced by extreme shifts in mood, energy and functioning.

Yes, now Bipolar Disorder is the clinically correct terminology for the dramatic, recycled changes experienced by individuals with this mental health disorder.  However, I must admit that manic-depressive held more meaning for me. It identified the two opposites of the continuum rather than using vague terminology as a label.

There are different variations of Bipolar Disorder listed in the two mental health diagnostic manuals, the DSM-IVtr (soon to become DSM-5) and the International Classification of Diseases (ICD-10).  Once thought to be a rare condition in children and youth, the 1990’s era saw a massive increase in Bipolar diagnoses for kids with severe sadness, irritability, anger, and grumpiness. a rise of 4000% in just 12 years!  As might be expected, the dramatic increase sparked discussion and disagreement about whether children were being misdiagnosed and then prescribed powerful psychotropic mediations with significant negative side effects. (A future topic for a B-List members)

Bipolar disorder is a life-long mental disability, but most research has shown that  kids diagnosed with childhood bipolar disorder (the expansive version) are no more likely to develop classic Bipolar Disorder than their non-diagnosed peers.  Additionally, the prescribed medications didn’t work as well in children as in adults.  Certainly, these youngsters possessed a legitimate mood disorder, one that may very well extend into adulthood. but for most of them, it wasn’t Bipolar Disorder.

One of the graduate students in my teacher preparation program in behavior disorders created a wonderful video regarding authentic Bi-Polar Disorder in children.  Using a case study of a 6 year old boy, Michelle then compares the youngster’s symptoms with the criteria for the condition, before offering strategies and approaches for intervention. (Thanks, Michelle!)

*Health note: Omega 3 oil, lecithin, and vitamins B6 & B12 have been implicated in the condition, with Bi-Polar individuals being deficient in these nutrients.  If you are seeking a natural alternative or supplement to Lithium and/or the other common medications you can find them in their purest form here: http://www.shop.com/healthnutrition-a.xhtml (Your purchases result in discounts & cash-back while supporting a kid’s pre-teen swim team.  My nutrition consultant, Cindy, is also available to assist you at this site)

A rose by any other name.

In response to the great controversy & disagreement as to whether this mental health disability should be diagnosed in kids, DSM-5 (due for distribution in May 2013) makes an effort to reduce the numbers of Bipolar diagnoses… by creating a new diagnosis!…: Distemper.  Oh Wait!!!  That’s my dog.  For our kids, the mental health diagnostic manual it will soon contain a new condition titled “Temper Dysregulation Disorder with Dysphoria” (TDD).

Dysphoria: An emotional state of feeling unwell or unhappy.

TDD displays itself in severe outbursts of anger/temper interchanging with negative mood states.  Unlike Bipolar Disorder, it does not include phases of mania (but neither did the criteria used to diagnose kids as having Bipolar Disorder… Odd, eh?… Labeling kids as being Bipolar when they didn’t have a second pole).  TDD is also not considered to be a life-long disorder.

The American Psychiatric Association states that it hopes that the majority of kids (perhaps 60-70%) who have or might have been diagnosed with Bipolar Disorder will now receive the TDD label.  This re-diagnosis would probably also include many youngsters with Conduct Disorder who were labeled as being Bipolar in order to obtain health insurance coverage for treatment

The symptoms of TDD in the upcoming DSM-5 manual are similar in many ways to the broad type of childhood bipolar disorder (as it was diagnosed). The proposed diagnostic criteria for TDD include:

severe recurrent temper outbursts that are grossly out of

proportion to the intensity of the situation

frequency of at least three temper outbursts per week

temper outbursts ongoing for at least one year

temper outbursts present in at least two settings (for

example, at home and at school)

onset before age 10

There is an excellent 10 minute video on the new disorder in the archives of National Public Radio: http://www.npr.org/player/v2/mediaPlayer.html?action=1&t=1&islist=false&id=123544191&m=123564957

FOR SCHOOL-BASED PERSONNEL

For those of you working with youngsters who have the symptoms mentioned above:

1. Rob Plevin’s 3-part FREE video series on working effectively with disruptive kids is still availabe.  Click here to view effective strategies for quieting noisy classes and kids.

2. Modify the character of the youngster using the Circle of Courage model of intervention.  This comprehensive, intensive and positive program changes lives.

3.  The Behavior Intervention Guide allows you to determine a disruptive youngster’s present level of readiness to change behaviour.  Based on the outcome of the assessment, strategies are provided that move the youngster toward greater levels of willingness to change his/her behavior for the better.

4.  Use “The Behavior Survival Guide for Kids: How to make good choices and stay out of trouble” in your social skills/anger management programs, or place it in the class library.  Stellar reviews by websites, magazines, parents, teachers, and the kids themselves let you know the effectiveness of this self-help book for kids.  It’s written on a 4th grade reading level… just like these weekly newletters!

5. Implement the FREE 100+ lesson plans that accompany The Behavior Survival Guide (or use them in isolation)

For Parents of Defiant & Angry Youngsters

1. Develop a home-school behavior change program based on the monetary system.  When money and priviledges are involved, kids listen!

2. Learn the principles of changing behaviour for the better, and effective strategies for helping your child make better behavior choices.

3.  Leave “The Behavior Survival Guide for Kids: How to make good choices and stay out of trouble” out on the coffee table for your child to pick up.

4. Seek out family counseling.

5. Acquire the comprehensive program designed specifically to help parents of children with Conduct Disorder/highly disobedient behavior change their child’s behavior for the better. (Click on the Total Transformation box below)

NEXT WEEK: Disruptive Behavior (Not otherwise specified)

(When the actions are disruptive, defiant, and/or aggressive,but don’t meet the criteria for ODD or Conduct Disorder)

Dr. Mac

Room 914west,

Department of Special Education, Hunter College,

695 Park Avenue,

New York,

NY 10021

Doctormac@BehaviorAdvisor.com

Retrieved from: http://www.behavioradvisor.com

Consequential Growth

In Fitness/Health, General Psychology, Happiness, Mindfulness, Well-being on Thursday, 14 February 2013 at 11:12

Consequential Growth

By: Timothy J. Wachtel

Written for the Texas Association for Adult Development & Aging

I’m older now. A little more pale, a little more frail, but I got my wits. The ebbs and flows of life have taken their course and have strewn me all over the place. It didn’t seem fair then and it doesn’t seem fair now. What do I have to show for it? I still try to keep my head held high and I smile a lot. Boy, life sure has a way of serving up its fair share of bumps and bruises . . . kinda glad in a way.

*****************************************

Have you ever found yourself in this reflective space? Have you ever not found yourself in this place? I think that everyone can agree that any individual who reaches the midpoint of adulthood and beyond is never immune to the trials and tribulations of life. It comes with the travel package. There always tend to be those pinnacle times of life; the times where the emotions get bruised, the spirit gets suffocated, the isolation looms large, the mind runs wild, and the rug from underneath you is no longer there. These life events and novel experiences come in many forms, as you very well know. Divorce, death of a family member, religious conversion, relocation, job transfer, job loss, injury or disease, natural disasters, kids move out, spouse goes off to war, traumatic stress, conflict; the list seems forever endless.

Is there a silver lining to all of this? I believe the answer is emphatically YES! We oftentimes don’t realize the goodness in these types of life events while we’re a part of the process. And it is a process; these situations, events, and experiences have a necessary starting point and oftentimes tend to be phases or stages throughout the process. Some people reach the productive end to the process, while others don’t quite reach the same successful terminal point. Today, science is doing more than ever before to inform us of these types of processes. More and more research is demonstrating evidence of the fact that many of these types of inexplicable occurrences in life result in very positive outcomes.

Research has found that individuals going through “troubled waters” over the course of a significant period of their lives tend to develop a greater sense of altruism and resilience, many experience more satisfaction or well-being in their life, and still others are finally able to come to terms with the meaning of their life. Scientists and practitioners use a battery of different terms to identify some of these events, some of which include: critical life eventsposttraumatic growthstress-related growthspiritual emergencytransformational crisisposttraumatic positive adjustmentgrowth through adversity, and the positive outcomes of one’s battle with Post-Traumatic Stress Disorder (PTSD).

I recently came up with a term that I believe helps to encapsulate the upsides to many of the downsides of life. “Consequential Growth” is the term I use to describe the results of these processes. Consequential Growth seems to semantically emphasize the necessary consequences we oftentimes experience throughout the growth process. The term broadly identifies the “dark nights” and the cognitive, spiritual, and emotional hardships we face during these times of duress.

Many books have been written on the positive results of these types of experiences in one’s life. Notably, the individual and collective works of Calhoun, Tedeschi, and Joseph talk much to these processes; especially in terms of Posttraumatic Growth. Moreover, many naturalistic and experimental research studies have found conclusive evidence of consequential growth. They inform us that those who are able to grow through their perceived negative experiences oftentimes maintain a more positive orientation toward life, are generally more optimistic, and tap into healthy coping strategies to get through the hardship(s). These individuals often have strong social circles and are seen by others as stronger and wiser as a result of going throughthe consequential growth process, even though they never signed-up for the turbulence.

The aging process is indeed complex. Life situations can catapult us right off our comfortable life. This is the stuff of character, wisdom, virtue, transformation, transcendence, higher consciousness, emotional resiliency, generativity and care for your fellow human beings. I wish you well on your next tumble.

References:

Tedeschi, Richard G.; Lawrence G. Calhoun (1995). Trauma and Transformation: Growing in the Aftermath of Suffering. SAGE Publications, Inc.
Joseph, Stephen (2011). What Doesn’t Kill Us: The New Psychology of Posttraumatic Growth. Basic Books
Timothy “Tim” J. Wachtel

Executive Director

The Center for Optimal Adult Development

www.optimaladult.org

Retrieved from: http://www.optimaladult.org/index.cfm/knowledge-center/coad-news-notes/consequential-growth/

 

wired for anxiety?

In Anxiety, Child/Adolescent Psychology, General Psychology, Psychiatry, School Psychology on Sunday, 10 February 2013 at 08:31

Are We All Just Wired for Anxiety?

By: Ben Michaels, Ph.D.

 Michael Shermer’s TEDTalk, “The Pattern Behind Self-deception” is both groundbreaking and earth-shattering. The neuroscience Shermer cites in his talk is tight, his examples are strong and his conclusions far-reaching. The implications that many have drawn from his talk regarding larger belief systems are beyond my expertise as a clinical psychologist and so I will (wisely or cowardly — you choose) sidestep these arguments.

I do however, think that one of the factors that Dr. Shermer stumbles upon in his talk has a wide applications for the field of clinical psychology, which is this:

If Shermer is right (and he is), and that our default setting is to see patterns where they don’t exist because the cost of being wrong (that there is no pattern) is usually much higher than the cost of being right (that there is a pattern) then I have some bad news for you:

We are all just wired for anxiety.

Let me break it down:

Let’s say something bad happens to us: We have a breakup, a breakdown, a trauma, an insult or injury of any kind. This leads us to seek out patterns in our environments that could signify the possibility of future pain. In fact, Shermer says that when we feel uncertain (like after a trauma) we will be even more prone to seeking out patterns, possibly seeing them where they don’t exist.

This desperate pattern seeking is, in essence, the pernicious spiral of anxiety: We are afraid of what’s next so our minds exit the present to try to solve an unsolveable math problem about our futures. The reason the problem is unsolveable is that all of the variables don’t yet exist. The key variable being the actual event.

If this tendency is our natural weakness, we must overcome it by using our natural strength: Thinking and testing our beliefs.

For example, I once worked with a handsome young man, who we will call, Nate, who was constantly told that he was “ugly” and “stupid” by his abusive father. When he first came to me, Nate was convinced that no woman would ever want to date him, let alone, marry him.

I responded to him by saying, maybe he’s right maybe no woman would have him, but there is only one way to find out: test his beliefs in the real world. I told him that if he asked out all the women in the world and none of them want to date him, than his anxiety would be justified If at least one woman wanted to then it would not be.

He realized that this was absurd, but after a great deal of relentless pushing, Nate agreed to try to approach a few women over time.

Fourteen months later he was engaged. He is now happily married and currently expecting his third child.

Science/Empiricism = 1; Anxiety/Fear = 0

The takeaway is this: We may indeed be wired for anxiety, but that does not mean that anxiety is our fate. If we use the gift of our minds well, we can overcome our wiring.

If you read this and are feeling anxious or are buried under the weight of any false belief because of your wiring, do the hard thing: Test it out. The only thing you have to lose is your anxiety!

Ideas are not set in stone. When exposed to thoughtful people, they morph and adapt into their most potent form. TEDWeekends will highlight some of today’s most intriguing ideas and allow them to develop in real time through your voice! Tweet #TEDWeekends to share your perspective or emailtedweekends@huffingtonpost.com to learn about future weekend’s ideas to contribute as a writer.

Retrieved from: http://www.huffingtonpost.com/ben-michaelis-phd/wired-for-anxiety_b_2599944.html?utm_source=linkedin&utm_medium=social&utm_content=2c773f97-31e5-4b88-bbb2-fa255a762ed1

Click here to read the original op-ed from the TED speaker who inspired the post and watch the TEDtalk below:

http://www.huffingtonpost.com/michael-shermer/what-is-skepticism-anyway_b_2581917.html?ir=TED+Weekends&ref=topbar

 

Human Needs, Buddhist Psychology and Mindfulness

In Buddhist Thoughts, General Psychology, Happiness, Mindfulness on Saturday, 19 January 2013 at 11:09

Human Needs, Buddhist Psychology and Mindfulness

Targeting mindfulness

Published on January 17, 2013 by Michael J. Formica, MS, MA, EdM in Enlightened Living

Buddhist psychology—and the Shankya yoga science from which it issues – describes seven psychological characteristics that inform our four life meta-categories (work, relationship, self and spirit) and also map directly to the various needs spectrums found in Western motivational psychology.

We can think of the life meta-categories of work, relationship, self and spirit as occurring in four quadrants. Within these quadrants are smaller categories, like job, love, sex, health, religion, etc., respectively. The way that each of us balances the four quadrants and their sub-categories creates a framework for our lives. To understand how and why we create that balance, we need to consider our underlying motivation.

Theories of human motivation abound. Most of us are familiar with Maslow’s hierarchy of needs, as well as Freud’s less rigidly presented spectrum of human needs. William McDougall, William James and Henry Murray have all contributed to this conversation, as has, more recently, Steven Reiss. In addition, Martin Seligman’s positive psychology would appear to be informed by Jung’s focus onspiritual fulfillment and Frankl’s will to meaning.

Whichever school of thought we subscribe to—whether the implied collection of needs suggested by Freud, the rigorous research of Reiss or the historically derived and empirically demonstrated strengths and virtues cited by Seligman—it is clear that human needs can be identified and that identification, allowing for some difference in perspective and labeling, is fairly consistent over time.

Buddhist psychology identifies seven psychological characteristics: life, order, wisdom, love, power, imagination, understanding and will. These were initially described in the Abhidharma, as well as the Rig Veda, and are remarkably similar to those found in the Western narrative compiled centuries later. Some map directly to the various Western systems and some more indirectly, but the relationship is consistently clear and reasonable.

If one were intent on drawing a direct line between the human needs spectrum described by Buddhist psychology and a Western counterpart, Seligman’s positive psychology would likely be the best choice. This is not so much because of any coincidence in the labeling scheme, but more because of the coincident perspective. Western psychology tends to issue from a place of damage and illness. Seligman’s work in positive psychology has been a relatively antithetical response to that position. Buddhist psychology would similarly have us start from a place of wholeness and perfection.

So, now we get to the question of mindfulness. What makes mindfulness a challenge is that there is no real starting point for witness consciousness, or the objective observation of the ‘Self’ by the ‘self’. That’s mainly because the self, or ego, interferes with that process by way of our assumptions, expectations and ideas about the way the world works. Applied mindfulness can be even more of a challenge because, once we get the meta-awareness of witness consciousness going, we need somewhere to point it and very often we don’t know where that is, exactly. So, we may be all “aware” and stuff, but often nothing really changes.

Now, getting back to needs, if we can gain an understanding of our needs and then unravel the dissonance around those needs we then have somewhere to point our mindfulness. The Reiss Motivational Profile, the Meyers-Briggs and the Enneagram are examples of tools that can help us to do this because they force us into a state of pseudo-witness consciousness by asking us to be objective observers of ourselves without (too much) interference from the ego.

For example—and we’ll use the Reiss Profile here because it is fairly clear and easy to follow—let’s say you’re experiencing feelings of an ongoing, non-clinical, free-floating, generalized anxiety. In layman’s terms, you’re freaking out a bit for no discernible reason.

You take the Reiss profile and discover (these are simplistic interpretations) you are Low Order (not much for structure), High Tranquility (don’t like chaos) and Low Vengeance (non-confrontational). You’re anxiety may well be, in part, derived from the fact that people who operate with little structure—don’t pick up after themselves, don’t pay bills on time, are tardy for work or social events–naturally invite both chaos and confrontation—messy house, late fees, irate bosses, coworkers, clients and friends.

An unaddressed dissonance around disparate needs creates psychic tension, which here we have labeled anxiety. If we want to backtrack into the Buddhist perspective, we could also say this dissonance is creating a disturbance in the muladhara and atala chakras and the manamaya kosha. This works because Western needs spectrums map quite easily to both the chakra and kosha systems found in the yoga Vedanta. But, I digress…

Without a direct perspective on your needs bias, you would likely point your mindfulness at the symptom (the anxiety)—and that can get a bit murky on both sides of the equation. With a more concrete notion of the source of the symptom, mindfulness techniques can be targeted. And that’s how we can loop back to witness consciousness.

Witness consciousness examines the state of the ‘self’ from the perspective of the ‘Self’. If we consider an understanding of our basic needs as a snapshot of the state of the ‘self’, then we have in hand the objective distance we need to effectively apply mindfulness where it is needed, rather than simply being generally—and likely less effectively—mindful.

© 2013 Michael J. Formica, All Rights Reserved

Retrieved from: http://www.psychologytoday.com/blog/enlightened-living/201301/human-needs-buddhist-psychology-and-mindfulness

 

The Year of the Suicide

In General Psychology on Thursday, 17 January 2013 at 06:19

The Year of the Suicide

Suicide rates among Americans are steadily rising and have been for years. Why are we killing ourselves?

BY KERA BOLONIK

Let’s call 2012 the year of the suicide: On Friday, the Department of the Army released a report revealing that suicides continue to outnumber combat-related deaths among American soldiers —an average of one suicide a day— a number that’s increasing despite the fact that the armed forces have installed new training and awareness programs over the past few years. Stateside, suicide has become theleading cause of death by injury, and is the 10th leading cause of death overall.According to a CDC report released over the summer, suicide attempts by high-school students has risen to from 6.3 percent in 2009 to 7.8 percent in 2011, and accounts for 13 percent of all deaths among people between the ages of 10 and 24 — the third leading cause of death in that age group.

These are sobering statistics. And with the statistics comes more data to explain them: The Washington Post reported that “the stress on the force after more than a decade of lengthy and multiple deployments for many troops in support of the wars in Iraq and Afghanistan,” while Defense Secretary Leon Panetta attributed the high rate to “substance abuse, financial distress and relationship problems … that will endure beyond war.” Among civilians, the number of suicides have been attributed to the recession — historically, there is a spike with every economic downturnAnd 20 percent of high-school teenagers say they are being bullied — 16 percent say they’ve been cyber-bullied through texting, IM-ing, email, and Facebook or other social media.

Though these stats may elicit sighs, we develop a kind of immunity to reading them because they’re so abstract — names are what humanize the story. And there were plenty in the headlines the past year, people we’ve admired from afar, or people we encountered because their suicides were so lurid. There were those who were said to have killed themselves to be released from physical agony, like “Soul Train’s” Don Cornelius, who battled unrelenting seizures from an aneurysm he’d had 15 years earlier, and Fleetwood Mac’s Bob Welch, who learned he’d suffer lifelong excruciating pain from the spinal surgery he’d had three months earlier. Director Tony Scott jumped off the Vincent Thomas Bridge in L.A., and was initially reported to have had inoperable brain cancer — though an autopsy would disprove that report (there was no sign of cancer). There were those who decided to end their lives because they were overcome with psychic pain, like “Three Cups of Tea” co-author David Oliver Relin, 49, and 57-year-old visual artist Mike Kelley, who had been suffering a depression following a breakup. It’s hard to know what motivated the most violent suicides, those paired with murder: Kansas City Chiefs linebacker Jovan Belcher, who shot himself, after having murdered his girlfriend, and Adam Lanza, who killed himself after committing one of the most heinous mass shootings in history.

There are so many angles, so many ways to explore this subject (and the news, I’m afraid, will provide us with plenty of opportunities): Has suicidal depression become an epidemic? Is suicide ever okay? Is this the fault of our health-care system? Would gun laws prevent suicide? Why are more and more suicides paired with homicides — and massacres? Each of these demands a dissertation. I’m not a psychiatrist or a policy wonk or a statistician, so I can’t even begin to answer these questions.

So I won’t. Instead, I come to this subject with a question driven by something very personal, a question that is at once the simplest and most complicated one to pose: Why do some of us choose to die, and some of us, even the depressed among us, have the will to live? There was a time when I believed I understood why people committed suicide. Yes, I’ve laid out some reasons above, about people I don’t know. But those responses are soundbites, given to the press by family members and friends of the deceased, or shrinks called on by the reporter, spokespeople for the organization that reps the deceased, etcetera. And while there is some truth to what they say, the fact is, probably none of us knows what finally pushed them over the edge. That is the legacy of suicide, the worst possible thing about it — that all of the surviving friends and family are sentenced to a life of torturous wonder.

I think about the grieving parents of Rutgers freshman Tyler Clementi, who killed himself in 2010. They were granted a sense of closure earlier this year, when the state of New Jersey’s Superior Court convicted Clementi’s roommate Dharun Ravi with 15 counts of crimes involving invasion of privacy and bias intimidation. The court’s ruling essentially gave the Clementis permission to believe that Ravi drove their son to kill himself. And indeed, Ravi was guilty of committing those crimes against Tyler Clementi, of creating a menacing environment. But was bullying what led Tyler to jump? It sounded plausible to me when the story broke. But then I read Ian Parker’s piece in The New Yorker last February, and I started to think otherwise.

Like Clementi, I went to Rutgers — I began my freshman year there 22 years before he did. I have no connection to New Jersey, though: I’d moved from Chicago, with the express purpose of coming out, in private, away from everyone I knew, after learning that they had one of the first gay and lesbian organizations on campus. Our situations were very different: I was outgoing and lived in the cultural epicenter of campus — a hotbed of activism, of activity, of everything. Clementi was a shy kid, bunking in a tiny room on an annex campus, Busch, living in exile as a lone gay among the engineering and math and pharmacy students who were not known, as a whole, for being socially progressive.

But he and I shared one thing: We pursued same-sex romantic partners who were deeply closeted. And few things can make you feel lonelier than not being able to enjoy and share love; what’s worse, contending with the mercurial temperament of a person terrified of exposure. It can match, if not exceed, the terror of being bullied: The threat of being dumped, of having to go through a breakup alone, can be more than enough to exacerbate any depressive’s sense of despair. I remember it well, because in those moments when my relationships threatened to come undone, my brain would feel like it was spinning off its axis, and my mind would switch into suicidal ideation mode, like a default, and my mood would plummet from elated to absolutely wanting to die.

But, something, I don’t know what, kept me from acting on my impulses: Instead, I’d call Lisa, my first friend at Rutgers, the one person I trusted to keep a secret, who happened to be the same person who could talk me out of it. According to Ian Parker’s New Yorker feature, Clementi, sadly, reached out only to people he’d met on a gay porn site, friends he’d never met in person. Which led me to imagine his thought process, based on my own: Following an argument with the lover, he’d become wholly absorbed in his toxic thoughts, fully rapt, even if momentarily, by his excruciating pain. But here’s where he and I would diverge: He’d snap and lapse into a fatal insanity that ultimately would propel toward the George Washington Bridge. And then …

Though it doesn’t matter what I imagine happened to Clementi. Because now I’m as guilty as any survivor of the dead, yearning for that closure, trying to create a linear narrative to make sense of the illogical — it’s what distinguishes the insane, murderous moment from the rational. But I do recognize those flashes of intense self-hatred that devolve into despondency. Fortunately, I never broke — in part, I like to think, because I was lucky enough to have a friend like Lisa. If only Lisa could have instilled in herself the same life-affirming message she instilled in her friends.

Three years after college graduation, I was in the grips of one of my most acute depressions. Unbeknownst to me at the time, so was Lisa. I’d returned home from an evening out with a friend, after having spent much of the week in bed, when I’d gotten a message that Lisa had hung herself. She was the last person I’d ever have expected to die by her own hand. In school, she was vibrant and brilliant, the friend from whom everyone sought advice (not just me) the friend who threw the most amazing dance parties — the friend who was, well, everybody’s best friend. But soon after we graduated, she developed an ailment I could only describe as a psychic cancer. I realize now, in retrospect, she was likely in the early stages of battling bipolar disorder, and after her second bout of a very intense, nearly catatonic depression, she killed herself, leaving behind people who would have done anything to save her: her fiancé, her parents, her older sister, and so many friends.

In the weeks after her suicide, I’d learned that she’d been very forthcoming about her suicidal ideations. In a way, it was hard not to see her incapacitating depression as a terminal illness, I rationalized, so why not forgive her for it the way we forgive stage-4 cancer patients for assisted suicides? I remember getting into it with my mother, who said suicide was the ultimate fuck you. “Well, that doesn’t apply to Lisa,” I barked. “She’s not an aggressive person, and she’s not a vindictive person!” And she wasn’t, not in the least. It wasn’t about hurting other people. It was just about hurting. I would say repeatedly, “I totally get this, I get why she did this.”

But in the years that followed, I saw how much it had hurt other people, especially her family: Her mother never recovered, and followed in her daughter’s footsteps eight years later. Which makes me think about the surviving families and friends of the soldiers and the football players, the teenagers and the luminaries: Maybe they have found a satisfactory answer, or maybe they saw it coming. But are those answers enough to stanch the grief? Or quiet the taunting, repeat-play interior monologue that asks whether something could have been done to stop it?

Now that I’m a 42-year-old mother, nearly 20 years after Lisa’s death, I admit: I no longer “get this” — and it terrifies me more than ever, as I cuddle with my toddler, who is walking and starting to talk and doing all the things 15-month-olds do. Because I think about the joy her parents must have felt in having two healthy, beautiful daughters, who thrived at school and in life, and I wonder, how does this tragic story fit in? It doesn’t. But it is their story now, and it tore apart a wonderful, loving family.

I can think of reasons — good reasons — why Tyler Clementi may have committed suicide. And Don Cornelius. And Tony Scott, and Jovan Belcher. But are those reasons the reason? Why wasn’t someone like Lisa able to carry on, and why is someone like me, who had been so outspokenly depressed, alive? I honestly have no idea. I can only say I’m grateful to Lisa for helping me stay here, even as I grieve for her, and for every single person who can’t bear to live another day.

Kera Bolonik is the arts editor of Salon. Follow her on Twitter @KeraBolonikMORE KERA BOLONIK.

Retrieved from: http://www.salon.com/2012/12/31/the_year_of_the_suicide/

know the statistics…

In Education, General Psychology, Humane Education, Personality Disorders, Pets, School Psychology, School violence on Sunday, 16 December 2012 at 12:47

http://www.incasa.org/PDF/2011/animal_human_violence.pdf

animal cruelty is not just animal cruelty…we all suffer.

In Animal Welfare, General Psychology, Humane Education, Personality Disorders, School violence on Saturday, 15 December 2012 at 07:03

i have long espoused the connection between animal cruelty and future deviant/violent behaviors.  i try to explain to those that might not have the same bleeding heart for animals and animal cruelty that i have (it guts me each and every time), should they not be concerned with the violence that the animals suffer (and i don’t really understand how not, but i am sure there are people who believe an animal is a creature for us to have dominion over and we can do what we please or that there are more important causes out there that need help and support), please take note, that choosing NOT to deal HARSHLY with this type of behavior will get us ALL in the long run.  it is said that most serial killers and school shooters were cruel to animals earlier in life.  to me, to ignore such behavior and play it off as something they will ‘grow out of ‘or a result of what is seen on tv, in movies, etc., is negligent knowing the statistics and predictive validity of such behaviors.  you see, those that are cruel to animals, more often than not, “graduate” to levels of cruelty that are inflicted not on animals, but on people.  so, should you not be incensed, disgusted, enraged, gutted, immensely saddened, etc….by the kid who set his dog on fire, or the kid who microwaved his cat, or the sheer magnitude of crimes inflicted upon animals daily with absolutely no regard for their suffering (there are so very many, and they are so very shocking, horrific, and born of pure evil)…should this not sicken you or move you into action, please…realize that at some point people will more likely than not have to deal with the aftermath of this cruelty when it extends to people.  

please, please, please…be aware, be vigilant, and above all, fight for stricter animal cruelty laws.  if not for the innocent animals, then for those that will be on the receiving end of the violence that stems from those that are able to inflict cruelty on animals.

http://jaapl.org/content/30/2/257.full.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2792040/

 

Early identification for individuals at risk for antisocial personality disorder

In General Psychology, School Psychology on Saturday, 15 December 2012 at 06:39

Early identification for individuals at risk for antisocial personality disorder

Jonathan Hill, MRCPsych

Abstract

Background Antisocial personality disorder is usually preceded by serious and persistent conduct problems starting in early childhood, and so there is little difficulty in identifying an at-risk group.

Aims To address six key areas concerning the relationship between early conduct problems and antisocial personality disorder.

Method Review of recent research into early identification of and intervention in child conduct problems, following up to possible adult antisocial behaviour.

Results Conduct problems are predictive of antisocial personality disorder independently of the associated adverse family and social factors. Prediction could be aided through identification of subtypes of conduct problems. There is limited evidence on which children have problems that are likely to persist and which will improve; children who desist from early conduct problems and those with onset in adolescence are also vulnerable as adults.

Conclusions The predictive power of the childhood precursors of antisocial personality disorder provides ample justification for early intervention. Greater understanding of subgroups within the broad category of antisocial children and adults should assist with devising and targeting interventions.

The identification of childhood precursors of adult psychiatric disorders offers the possibility of early intervention and hence prevention. In the case of antisocial personality disorder the early indicators are remarkably clear. Starting with Robins’ (1966) classic follow-up of children referred to a clinic for conduct problems, numerous studies have shown that persistent and pervasive aggressive and disruptive behaviours seen before the age of 11 years are strongly associated with persistence of antisocial behaviours through adolescence and into adult life. As Robins described, the risk extends far beyond antisocial behaviours to unstable relationships, unreliable parenting and underachievement in education and at work (Moffitt et al, 2002). This broad constellation of difficulties is reflected in DSM—IV antisocial personality disorder (American Psychiatric Association, 1994). Furthermore, children who do not have conduct problems are very unlikely to subsequently develop antisocial personality disorder (which is rare without a history of conduct problems). Conduct disorder is a specific diagnosis within DSM—IV, which requires antisocial acts seen generally in older children and adolescents. In this paper the terms ‘conduct problems’ and ‘the conduct disorders’ are used to denote serious oppositional, aggressive or antisocial behaviours whether or not they meet DSM criteria for conduct disorder.

METHOD

Selective review of findings published over the past 10 years in childhood predictors of antisocial personality disorder, and consideration of issues still to be addressed in relation to early identification of individuals at risk.

RESULTS

Clinical policy

From a clinical and policy perspective, the strength of the continuity from conduct problems to antisocial personality disorder is ample grounds for making strenuous efforts to prevent the appearance of aggressive and disruptive behaviours in young children, and to intervene early once they have been identified. It is not the purpose of this paper to review the evidence for the effectiveness of prevention programmes and of early interventions for conduct problems, but a brief summary highlights the need for further refinements in early identification. A small number of adequately designed randomised controlled trials of preventive programmes to reduce conduct problems have been carried out, some of which have yielded promising results. Equally, whereas there have been some significant improvements, often the effects have been quite small; and some studies have shown no benefits (LeMarquand et al, 2001). There is substantial support for the effectiveness of parent management training programmes in reducing overall levels of conduct problems in children (Kazdin, 2000), and for the effectiveness of stimulants where conduct problems are associated with attention-deficit hyperactivity disorder (ADHD) (Swanson et al, 2001). Nevertheless, there has been considerable variability in outcomes. Parent training has been found to be less effective for the higher-risk families characterised by socio-economic disadvantage, marital discord or single parent status, high parental stress and maternal unresolved loss or trauma (Routh et al, 1995Kazdin, 1997). Children with more severe or chronic problems or with comorbid conditions are less likely to do well (Ruma et al, 1996). Evidence of the long-term effectiveness of psychosocial treatments for conduct problems, and of stimulants for conduct problems comorbid with ADHD, is lacking.

Early identification

It may be that the problem will be solved simply through better treatment techniques; however, attention to six issues in early identification may also be of value in generating ideas for the development of interventions. First, conduct problems in young children are associated with many other adverse factors such as ineffective parenting practices, discordant and unstable families, poor peer relationships and educational failure. It is important to clarify whether it is the child’s disorder that requires early identification, or these associated factors or both. Second, conduct problems in childhood are generally identified on the basis of a broad cluster of behaviours. The identification of subtypes may lead to a better understanding of underlying mechanisms, and hence to improved matching of treatment to clinical needs. Third, in approximately 50% of children with early conduct problems these do not persist into adolescence and adult life. Ways of distinguishing persisters and desisters are needed. Fourth, given the intractability of behaviour problems in some young children, we need to ask whether identification at an earlier age is possible. Fifth, the adult outcomes of children who show early conduct problems and then desist, and of those whose problems start in adolescence, need to be considered. Finally, we need to attend to the adult outcomes that we are attempting to anticipate. It may be that specific antisocial outcomes have different antecedents from those of antisocial personality disorder.

What is predictive?

It is possible that, because conduct problems are associated with a wide range of adverse individual, family and social factors, the conduct problems per seare not the antecedents of antisocial personality disorder but are markers for these other difficulties that are the true antecedents. In general, the evidence supports conduct problems as true antecedents (Farrington et al, 1990). For example, studies that have assessed both conduct problems and quality of peer relationships, and then followed children over several years, have consistently found that early conduct problems predict later antisocial behaviours (Tremblay et al, 1995Woodward & Fergusson, 1999). By contrast, the role of peer relationships has been less clear. This should not, however, be interpreted to mean that the associated factors are unimportant. For example in the Dunedin Multidisciplinary Health and Development Study, violent crime at the age of 18 years was predicted by the combination of temperamental lack of control (quick to show negative emotions when frustrated, poor impulse control) and number of changes of parental figure before the age of 13 years, which probably reflected a range of family adversities (Henry et al, 1996).

Sources of heterogeneity in the conduct disorders

Longitudinal studies from childhood to adulthood have used a wide range of ways to characterise conduct problems. Generally they have made use of summary scores generated from a range of questionnaires completed by teachers and parents (Farrington et al, 1990Fergusson et al, 1996Moffitt et al, 1996). The consistency of the findings may suggest that it does not matter much how the problem is defined. Equally, there are pointers to potentially important kinds of heterogeneity. Children with conduct problems and hyperactivity/inattention differ from those with ‘ pure’ conduct disorder in that their problems are more severe and likely to persist, and they are more likely to have neuropsychological deficits (Lynam, 1996). Lynam (1998) has argued that children with attention-deficit hyperactivity problems are ‘fledgling psychopaths’, implying that they are more likely to show in adult life the combination of callousness, superficial charm and antisocial behaviour that characterises a sub-group of adults with antisocial personality disorder. Frick and colleagues give priority to callous—unemotional traits in childhood. In a series of studies they have demonstrated that children with antisocial problems who exhibit these traits differ from other children with antisocial problems (Barry et al, 2000) in apparently having fewer verbal deficits (Loney et al, 1998) and in coming from families that are not characterised by dysfunctional parenting practices seen generally in the conduct disorders (Wootton et al, 1997). Children exhibiting callous—unemotional traits may also have a deficit in processing behavioural evidence of distress in others. Associations between scores assessing callous and unemotional characteristics and a reduced ability to recognise fear and sadness have been shown in young adolescents recruited in mainstream schools and children with identified emotional and behavioural problems (Blair & Coles, 2003;Stevens et al, 2001).

Loeber et al (1993) have proposed that three contrasting patterns of childhood antisocial problems reflect different pathways for different behaviour patterns: an ‘overt’ pathway characterised by bullying, followed by early fighting and proceeding to more serious violence; a ‘covert’ pathway starting with lying and stealing, and going on to more serious damage to property; and an ‘ authority conflict’ pathway in which oppositional and defiant behaviours are prominent.

A further distinction, between ‘reactive’ and ‘ proactive’ antisocial behaviours, cuts across this three-category typology. Reactive acts occur in response to actual or perceived threat from others, whereas proactive behaviours are initiated by the individuals (Dodge & Coie, 1987). Reactive aggression is thought to involve angry retaliation, in contrast to the cold unprovoked calculation of proactive aggression. Dodge et al (1997) reported that, compared with children showing proactive aggression, ‘reactive’ children were more likely to have been physically abused, to have poor peer relationships, to have shown aggression from an earlier age and to have attention-deficit and hyperactivity symptoms. A central idea in Dodge’s model is that reactive aggression is mediated by a readiness to perceive hostile intent in the actions of others. However, the evidence for this is inconsistent. At this stage these can be considered as promising subtypes that may lead to a more precise specification of mechanisms, and hence provide pointers to different kinds of intervention. Longitudinal studies to determine whether they differ in course are needed.

Who are the persisters and desisters?

We have already referred to the poor outlook of children with both conduct disorder and ADHD symptoms. On the basis of retrospective reports within a large epidemiological study, Robins & Price (1991) found that the number of childhood antisocial problems is associated with risk of antisocial personality disorder. Studies within childhood provide some further clues regarding risk of persistence. Loeber et al (2000) found that early fighting and hyperactivity predicted persistence of antisocial behaviours over a 6-year period among boys referred for conduct problems. In a prospective study of a representative general population sample from ages 7-9 years to 14-16 years, persisters had the highest levels of family adversity and lower IQ and self-esteem (Fergussonet al, 1996). Children with early conduct problems that did not persist had levels of these risk factors that were intermediate between those of persisters and of children who lacked early behavioural problems. Persisters were more likely than those whose early antisocial behaviours had remitted to have a deviant peer group in adolescence. Whether this was a reflection or a cause of persistence is not clear; however, it is consistent with Sampson and Laub’s argument that a key factor in determining persistence may be the presence or absence of social bonds and controls (Sampson & Laub, 1994).

Earlier predictors

We might suppose that, given the stability of conduct problems from the age of 3 years onwards, earlier precursors should be readily identifiable. However, the findings have been inconsistent. For example, the idea has been extensively investigated that early ‘difficult’ temperament, comprising traits such as predominantly negative emotions and ready frustration, contributes to irritable parenting, which in turn increases the risk for conduct problems. Studies using assessments of temperament based on parental reports have yielded some positive findings, but these are vulnerable to parental attributions. Recent studies have failed to demonstrate consistently that observational measures of temperament made in the first year of life predict later conduct problems (Belsky et al, 1998Aguilar et al, 2000). Early attachment difficulties might be expected to increase the risk for later conduct problems. Here again the evidence is not convincing (Hill, 2002). It is likely that the quality of parenting in infancy is predictive of later conduct problems (Belsky et al, 1998) and it may be that the most promising approaches to the identification of early predictors will examine specific interactions between infant characteristics and early social experience (Shaw et al, 1996Belsky et al, 1998).

Desisters and later onsets

We have focused so far on boys who show early conduct problems that persist into adult life. It has generally been assumed that those whose conduct problems remit have ‘recovered’. However, recent evidence from the Dunedin Study suggests that although these children are not at increased risk for antisocial outcomes, they are by no means free of difficulties (Moffitt et al, 2002). At the age of 26 years they had higher rates of depression and anxiety disorders, both self- and informant-rated, and they were socially isolated, with few friends. They shared the poor educational and work records of the life-course persistent group who were antisocial as adults. Likewise, those with onset in adolescence, provisionally termed by Moffitt ‘ adolescence limited’, were not free of problems by the age of 26 years. Compared with those who were not significantly antisocial in childhood or adolescence, these young men had higher rates of documented and self-reported drug and property crimes, and their informants reported more depression and anxiety symptoms.

Heterogeneity within antisocial personality disorder

Thus far in this paper the assumption has been made that the DSM-IV antisocial personality disorder category best summarises the antisocial outcomes of interest. There is little doubt that it succeeds as a broad-brush characterisation of antisocial behaviour and associated wider social dysfunction. However, it lacks specificity. In common with all DSM diagnoses, it requires the presence of a number of maladaptive behaviours or mental states identified from a larger set. Hence, the requirements can be met in numerous ways. This may limit the investigation of more specific causal factors, and so a more precise specification of the adult antisocial outcomes may be needed.

The identification of ‘psychopathic disorder’ makes the point. DSM-IV antisocial personality disorder is present in 50-80% of convicted offenders, but a much smaller group of 15-30% are judged to have characteristics such as grandiosity, callousness, deceitfulness, shallow affect and lack of remorse (Hart & Hare, 1989). These individuals are more likely than other offenders to have a history of severe and violent offences, and they may also have a distinctive deficit in interpersonal sensitivity. In a comparison of prisoners with and without psychopathic disorder, the groups did not differ in their ability to attribute correctly happiness, sadness and embarrassment to protagonists in short stories. However, in response to guilt stories, those with psychopathic disorder were more likely to attribute happiness or indifference to the protagonists (Blair et al, 1995). It has been proposed that psychopathy is associated with a failure to inhibit aggression in response to signs of distress in others, arising from a deficit in processing behavioural evidence of that distress (Blair et al, 1997). There is supportive evidence that, compared with other offenders, adults with psychopathic disorder have reduced autonomic responses to distress cues (Chaplin et al, 1995Blair et al, 1997). As we saw earlier, a subgroup of children with antisocial problems who exhibit callous—unemotional traits has been identified that may parallel adults with psychopathic disorder. No studies have yet tested for continuity between child and adult psychopathic traits by following these children into adult life.

DISCUSSION

Children at risk for future antisocial personality disorder are readily identified, but evidence on the long-term effectiveness of prevention and treatment programmes is limited. Some progress has been made in identifying subgroups of children with antisocial problems in which different causal processes operate, and therefore for which there are different treatment needs. The available research does not yet tell us whether differences in the patterning, or associated features, of childhood conduct problems are predictive of distinctive adult outcomes. If is possible that this review was subject to selection bias.

Clinical Implications and Limitations

CLINICAL IMPLICATIONS

  • The identification and treatment of conduct problems in early childhood are central to the prevention of antisocial personality disorder.
  • The conduct disorders are heterogeneous in the patterning and course of symptoms, with implications for matching treatment to type of problem.
  • There is considerable heterogeneity within antisocial personality disorder, so that there is a need to identify specific early indicators of particular adult antisocial outcomes.

LIMITATIONS

  • Most of the research reviewed in the article refers to antisocial personality disorder in males.
  • Few longitudinal studies of general populations have included sufficient numbers of antisocial children to explore heterogeneity.
  • Little is known about very early indicators of children at risk for the development of conduct problems.

Footnotes

  • * Paper presented at the second conference of the British and Irish Group for the Study of Personality Disorders (BIGSPD), University of Leicester, UK, 31 January to 3 February 2001.

References

  1. Aguilar, B., Sroufe, L. A., Egeland, B., et al (2000) Distinguishing the early-onset/persistent and adolescence-onset antisocial behaviour types: from birth to sixteen years. Development and Psychopathology12, 109-132.
  1. American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM-IV). Washington, DC: APA.
  1. Barry, C. T., Frick, P. J., DeShazo, T. M., et al (2000) The importance of callous—unemotional traits for extending the concept of psychopathy to children. Journal of Abnormal Psychology109, 335 -340.
  1. Belsky, J., Hsieh, K-H. & Crnic, K. (1998) Mothering, fathering, and infant negativity as antecedents of boys’ externalising problems and inhibition at age 3 years: differential susceptibility to rearing experience?Development and Psychopathology10, 301 -320.
  1. Blair, R. J. R. & Coles, M. (2003) Expression recognition and behavioural problems of early adolescence. Cognitive Development, in press.
  1. Blair, R. J. R., Sellars, C., Strickland, I., et al (1995) Emotion attributions in psychopathy. Personality and Individual Differences19, 431-437.
  1. Blair, R. J. R., Jones, L., Clark, F., et al (1997) The psychopathic individual: a lack of responsiveness to distress cues? Psychophysiology34,192 -198.
  1. Chaplin, T. C., Rice, M. E. & Harris, G. T. (1995) Salient victim suffering and perceptual responses of child molesters. Journal of Consulting and Clinical Psychology63, 249 -255.
  1. Dodge, K. A. & Coie, J. D. (1987) Social information-processing factors in reactive and proactive aggression in children’s peer groups. Journal of Personality and Social Psychology53, 1146 -1157.
  1. Dodge, K. A., Lochman, J. E., Harnish, J. D., et al (1997) Reactive and proactive aggression in school children and psychiatrically impaired chronically assaultative youths. Journal of Abnormal Psychology106,37-51.
  1. Farrington, D. P., Loeber, R. & Van Kammen, W. B. (1990) Long-term criminal outcomes of hyperactivity—impulsivity—attention-deficit and conduct problems in childhood. In Straight and Devious Pathways from Childhood to Adulthood (eds L. N. Robins & M. R. Rutter), pp. 62 -81. New York: Cambridge University Press.
  1. Fergusson, D. M., Lynskey, M. T. & Horwood, L. J. (1996) Factors associated with continuity and changes in disruptive behaviour patterns between childhood and adolescence. Journal of Abnormal Psychology24,533 -553.
  2. Hart, S. D. & Hare, R. D. (1989) Discriminant validity of the Psychopathy Checklist in a forensic psychiatric population. Psychological Assessment: A Journal of Consulting and Clinical Psychology1, 211 -218.
  1. Henry, B., Caspi, A., Moffitt, T. E., et al (1996) Temperamental and familial predictors of violent and non-violent criminal convictions: from age 3 to age 18. Development Psychopathology32, 614 -623.
  1. Hill, J. (2002) Biological, psychological and social processes in the conduct disorders. Journal of Child Psychiatry and Psychology43, 133 -164.
  1. Kazdin, A. E. (1997) Parent management training: evidence, outcomes and issues. Journal of the American Academy of Child and Adolescent Psychiatry36, 1349 -1356.
  1. Kazdin, A. E. (2000) Treatment of conduct disorders. In Conduct Disorders in Childhood and Adolescence (eds J. Hill & B. Maughan). Cambridge: Cambridge University Press.
  1. LeMarquand, D., Tremblay, R. & Vitaro, R. (2001) The prevention of conduct disorder: a review of successful and unsuccessful experiments. InConduct Disorders in Childhood and Adolescence (eds J. Hill & B. Maughan). Cambridge: Cambridge University Press.
  1. Loeber, R., Wung, P., Keenan, K., et al (1993) Developmental pathways in disruptive child behaviour. Development and Psychopathology,5, 101-132.
  1. Loeber, R., Green, S. M., Lahey, B. B., et al (2000) Physical fighting in childhood as a risk factor for later mental health problems. Journal of the American Academy of Child and Adolescent Psychiatry39, 421 -428.
  2. CrossRefMedline
  1. Loney, B. R., Frick, P. J., Ellis, M., et al (1998) Intelligence, psychopathy, and antisocial behaviour. Journal of Psychopathology and Behavioural Assessment20, 231 -247.
  1. Lynam, D. R. (1996) The early identification of chronic offenders: who is the fledgling psychopath? Psychological Bulletin120, 209 -234.
  1. Lynam, D. R. (1998) Early identification of the fledgling psychopath: locating the psychopathic child in the current nomenclature. Journal of Abnormal Psychology107, 566 -575.
  1. Moffitt, T. E., Caspi, A., Dickson, N., et al (1996) Childhood-onset versus adolescent-onset antisocial conduct in males: natural history from 3 to 18. Development and Psychopathology8, 399 -424.
  1. Moffitt, T. E., Caspi, A., Harrington, H., et al (2002) Males on the life-course persistent and adolescence-limited antisocial pathways: follow-up at age 26. Development and Psychopathology14, 179 -207.
  1. Robins, L. N. (1966) Deviant Children Grown-Up: A Sociological and Psychiatric Study of Sociopathic Personalities. MD: Williams and Wilkins.
  1. Robins, L. N. & Price, R. K. (1991) Adult disorders predicted by childhood conduct problems: results from the NIMH Epidemiological Catchment Area Project. Psychiatry542, 116 -132.
  1. Routh, C. P., Hill, J. W., Steele, H., et al (1995) Maternal attachment status, psychosocial stressors and problem behaviour: follow-up after parent training courses for conduct disorder. Journal of Child Psychology and Psychiatry36, 1179 -1198.
  1. Ruma, P. R., Burke, R. V. & Thompson, R. W. (1996) Group parent training: is it effective for children of all ages? Behavior Therapy27, 159-169.
  1. Sampson, R. J. & Laub, J. H. (1994) Urban poverty and the family context of delinquency: a new look at structure and process in a classic study. Child Development65, 523 -540.
  1. Shaw, D. S., Owens, E. B., Vondra, J. I., et al (1996) Early risk factors and pathways in the development of early disruptive behavioural problems.Development and Psychopathology8, 679 -700.
  1. Stevens, D., Charman, T. & Blair, R. J. R. (2001) Recognition of emotion in facial expressions and vocal tones in children with psychopathic tendencies. Journal of Genetic Psychology162, 201 -211.
  1. Swanson, J. M., Kraemer, H. C., Hinshaw, S. P., et al (2001) Clinical relevance of the primary findings of the MTA: success rates based on severity of ADHD and ODD symptoms at the end of treatment. Journal of the American Academy of Child and Adolescent Psychiatry40, 168 -179.
  1. Tremblay, R. E., Masse, L. C., Vitaro, F., et al (1995) The impact of friends’ deviant behaviour on early onset of delinquency: longitudinal data from six to thirteen years of age. Development and Psychopathology7,649-668.
  1. Woodward, L. J. & Fergusson, D. M. (1999) Childhood peer relationship problems and psychosocial adjustment in late adolescence.Journal of Abnormal Child Psychology27, 87-104.
  1. Wooton, J. N., Frick, P. J., Shelton, K. K., et al (1997) Ineffective parenting and childhood conduct problems: the moderating role of callous—unemotional traits. Journal of Consulting and Clinical Psychology65, 301-308.

i have no words right now…

In General Psychology, School Psychology, School violence, Uncategorized on Friday, 14 December 2012 at 17:14

http://www.neahin.org/blog/school-crisis-resources.html

http://www.neahin.org/educator-resources/school-crisis-guide.html

DSM-V…pick and choose

In General Psychology on Thursday, 6 December 2012 at 13:18

DSM-5 Is a Guide Not a Bible: Simply Ignore Its Ten Worst Changes

Allen Frances, Professor Emeritus, Duke University

This is the saddest moment in my 45 year career of studying, practicing, and teaching psychiatry. The Board of Trustees of the American Psychiatric Association has given its final approval to a deeply flawed DSM-5 containing many changes that seem clearly unsafe and scientifically unsound. My best advice to clinicians, to the press, and to the general public — be skeptical and don’t follow DSM-5 blindly down a road likely to lead to massive over-diagnosis and harmful over-medication. Just ignore the 10 changes that make no sense.

Brief background. DSM-5 got off to a bad start and was never able to establish sure footing. Its leaders initially articulated a premature and unrealizable goal — to produce a paradigm shift in psychiatry. Excessive ambition combined with disorganized execution led inevitably to many ill-conceived and risky proposals.

These were vigorously opposed. More than 50 mental health professional associations petitioned for an outside review of DSM-5 to provide an independent judgment of its supporting evidence and to evaluate the balance between its risks and benefits. Professional journals, the press, and the public also weighed in — expressing widespread astonishment about decisions that sometimes seemed not only to lack scientific support but also to defy common sense.

DSM-5 has neither been able to self correct nor willing to heed the advice of outsiders. It has instead created a mostly closed shop — circling the wagons and deaf to the repeated and widespread warnings that it would lead to massive misdiagnosis. Fortunately, some of its most egregiously risky and unsupportable proposals were eventually dropped under great external pressure (most notably ‘psychosis risk,’ mixed anxiety/depression, Internet and sex addiction, rape as a mental disorder, ‘hebephilia,’ cumbersome personality ratings, and sharply lowered thresholds for many existing disorders). But APA stubbornly refused to sponsor any independent review and has given final approval to the 10 reckless and untested ideas that are summarized below.

The history of psychiatry is littered with fad diagnoses that in retrospect did far more harm than good. Yesterday’s APA approval makes it likely that DSM-5 will start a half or dozen or more new fads which will be detrimental to the misdiagnosed individuals and costly to our society.

The motives of the people working on DSM-5 have often been questioned. They have been accused of having a financial conflict of interest because some have (minimal) drug company ties and also because so many of the DSM-5 changes will enhance Pharma profits by adding to our already existing societal overdose of carelessly prescribed psychiatric medicine. But I know the people working on DSM-5 and know this charge to be both unfair and untrue. Indeed, they have made some very bad decisions, but they did so with pure hearts and not because they wanted to help the drug companies. Their’s is an intellectual, not financial, conflict of interest that results from the natural tendency of highly specialized experts to over value their pet ideas, to want to expand their own areas of research interest, and to be oblivious to the distortions that occur in translating DSM-5 to real life clinical practice (particularly in primary care where 80 percent of psychiatric drugs are prescribed).

The APA’s deep dependence on the publishing profits generated by the DSM-5 business enterprise creates a far less pure motivation. There is an inherent and influential conflict of interest between the DSM-5 public trust and DSM-5 as a best seller. When its deadlines were consistently missed due to poor planning and disorganized implementation, APA chose quietly to cancel the DSM-5 field testing step that was meant to provide it with a badly needed opportunity for quality control. The current draft has been approved and is now being rushed prematurely to press with incomplete field testing for one reason only — so that DSM-5 publishing profits can fill the big hole in APA’s projected budget and return dividends on the exorbitant cost of 25 million dollars that has been charged to DSM-5 preparation.

This is no way to prepare or to approve a diagnostic system. Psychiatric diagnosis has become too important in selecting treatments, determining eligibility for benefits and services, allocating resources, guiding legal judgments, creating stigma, and influencing personal expectations to be left in the hands of an APA that has proven itself incapable of producing a safe, sound, and widely accepted manual.

New diagnoses in psychiatry are more dangerous than new drugs because they influence whether or not millions of people are placed on drugs — often by primary care doctors after brief visits. Before their introduction, new diagnoses deserve the same level of attention to safety that we devote to new drugs. APA is not competent to do this.

So, here is my list of DSM-5’s 10 most potentially harmful changes. I would suggest that clinicians not follow these at all (or, at the very least, use them with extreme caution and attention to their risks); that potential patients be deeply skeptical, especially if the proposed diagnosis is being used as a rationale for prescribing medication for you or for your child; and that payers question whether some of these are suitable for reimbursement. My goal is to minimize the harm that may otherwise be done by unnecessary obedience to unwise and arbitrary DSM-5 decisions.

1) Disruptive Mood Dysregulation Disorder: DSM-5 will turn temper tantrums into a mental disorder — a puzzling decision based on the work of only one research group. We have no idea how this untested new diagnosis will play out in real life practice settings, but my fear is that it will exacerbate, not relieve, the already excessive and inappropriate use of medication in young children. During the past two decades, child psychiatry has already provoked three fads — a tripling of Attention Deficit Disorder, a more than 20-times increase in Autistic Disorder, and a 40-times increase in childhood Bipolar Disorder. The field should have felt chastened by this sorry track record and should engage itself now in the crucial task of educating practitioners and the public about the difficulty of accurately diagnosing children and the risks of over-medicating them. DSM-5 should not be adding a new disorder likely to result in a new fad and even more inappropriate medication use in vulnerable children.

2) Normal grief will become Major Depressive Disorder, thus medicalizing and trivializing our expectable and necessary emotional reactions to the loss of a loved one and substituting pills and superficial medical rituals for the deep consolations of family, friends, religion, and the resiliency that comes with time and the acceptance of the limitations of life.

3) The everyday forgetting characteristic of old age will now be misdiagnosed as Minor Neurocognitive Disorder, creating a huge false positive population of people who are not at special risk for dementia. Since there is no effective treatment for this ‘condition’ (or for dementia), the label provides absolutely no benefit (while creating great anxiety) even for those at true risk for later developing dementia. It is a dead loss for the many who will be mislabeled.

4) DSM-5 will likely trigger a fad of Adult Attention Deficit Disorder leading to widespread misuse of stimulant drugs for performance enhancement and recreation and contributing to the already large illegal secondary market in diverted prescription drugs.

5) Excessive eating 12 times in 3 months is no longer just a manifestation of gluttony and the easy availability of really great tasting food. DSM-5 has instead turned it into a psychiatric illness called Binge Eating Disorder.

6) The changes in the DSM-5 definition of autism will result in lowered rates — 10 percent according to estimates by the DSM-5 work group, perhaps 50 percent according to outside research groups. This reduction can be seen as beneficial in the sense that the diagnosis of autism will be more accurate and specific — but advocates understandably fear a disruption in needed school services. Here the DSM-5 problem is not so much a bad decision, but the misleading promises that it will have no impact on rates of disorder or of service delivery. School services should be tied more to educational need, less to a controversial psychiatric diagnosis created for clinical (not educational) purposes and whose rate is so sensitive to small changes in definition and assessment.

7) First time substance abusers will be lumped in definitionally in with hard-core addicts despite their very different treatment needs and prognosis and the stigma this will cause.

8) DSM-5 has created a slippery slope by introducing the concept of Behavioral Addictions that eventually can spread to make a mental disorder of everything we like to do a lot. Watch out for careless overdiagnosis of Internet and sex addiction and the development of lucrative treatment programs to exploit these new markets.

9) DSM-5 obscures the already fuzzy boundary been Generalized Anxiety Disorder and the worries of everyday life. Small changes in definition can create millions of anxious new ‘patients’ and expand the already widespread practice of inappropriately prescribing addicting anti-anxiety medications.

10) DSM-5 has opened the gate even further to the already existing problem of misdiagnosis of PTSD in forensic settings.

DSM-5 has dropped its pretension to being a paradigm shift in psychiatric diagnosis and instead (in a dramatic 180 degree turn) now makes the equally misleading claim that it is a conservative document that will have minimal impact on the rates of psychiatric diagnosis and in the consequent provision of inappropriate treatment. This is an untenable claim that DSM-5 cannot possibly support because, for completely unfathomable reasons, it never took the simple and inexpensive step of actually studying the impact of DSM on rates in real world settings.

Except for autism, all the DSM-5 changes loosen diagnosis and threaten to turn our current diagnostic inflation into diagnostic hyperinflation. Painful experience with previous DSMs teaches that if anything in the diagnostic system can be misused and turned into a fad, it will be. Many millions of people with normal grief, gluttony, distractibility, worries, reactions to stress, the temper tantrums of childhood, the forgetting of old age, and ‘behavioral addictions’ will soon be mislabeled as psychiatrically sick and given inappropriate treatment.

People with real psychiatric problems that can be reliably diagnosed and effectively treated are already badly shortchanged. DSM-5 will make this worse by diverting attention and scarce resources away from the really ill and toward people with the everyday problems of life who will be harmed, not helped, when they are mislabeled as mentally ill.

Our patients deserve better, society deserves better, and the mental health professions deserve better. Caring for the mentally ill is a noble and effective profession. But we have to know our limits and stay within them.

DSM-5 violates the most sacred (and most frequently ignored) tenet in medicine — First Do No Harm! That’s why this is such a sad moment.

Retrieved from: http://www.huffingtonpost.com/allen-frances/dsm-5_b_2227626.html?utm_source=Alert-blogger&utm_medium=email&utm_campaign=Email%2BNotifications

DSM-V…out with the old and in with the new…

In Autism Spectrum Disorders, General Psychology, Psychiatry, School Psychology on Thursday, 6 December 2012 at 11:20

http://www.cbsnews.com/8301-204_162-57556754/aspergers-syndrome-dropped-from-american-psychiatric-association-manual/

more controvery regarding the dsm-v…

In General Psychology on Sunday, 2 December 2012 at 11:46

DSM-5 R.I.P?

Yesterday, the proposed new DSM-5 revision of the American Psychiatric Associations “Bible of Psychiatry” came under yet more criticism.

Aaron T. Beck, the father of currently-mega-popular cognitive behavioural therapy,started it off with an attack on the upcoming changes to one diagnosis, Generalized Anxiety Disorder; but many of the points also apply to the other DSM-5 proposals:

The lack of specific features, which is the primary issue for GAD, will not be addressed in DSM-5. The hallmark of the condition will remain pathological worry, although it also characterizes other disorders. Likewise, the proposed behavioral diagnostic criteria lack specificity for GAD, and it is not clear how these will be assessed. The proposed changes will lower the diagnostic threshold for GAD in DSM-5… many currently subthreshold cases will qualify for this diagnosis. The likely inclusion of many such “false-positives” will result in an artificial increase in the prevalence of GAD and will have further negative consequences.

Then from across the Atlantic, and also across the psychotherapy-vs-medication divide, came another piece of criticism. The authors are all associated with the European Medicines Agency (EMA, Europe’s equivalent of the FDA), or with national drug regulators. Although they’re writing in a personal capacity, this is still big news if you ask me.

These authors start out by saying that the EMA is broadly in favour of DSM reform, but they then attack one of the key DSM-5 innovations – the move towards ‘dimensional measures‘ of symptoms in addition to diagnoses:

One of our main concerns is related to potential future [drug] indications based on an effect on a dimension that is independent of diagnostic categories (although we acknowledge that non-specific claims are common in other areas, such as analgesics for pain). As an example, cognitive impairments are common in psychiatric disorders, but they do not have a unique clinical pattern or a unitary cause.

 

We therefore believe that, at present, such a cross-cutting approach may increase heterogeneity in patient populations and make the assessment of the benefit–risk balance more difficult. Similarly, the use of dimensions as key secondary end points in many different diagnostic categories may lead to pseudospecific indications and polypharmacy. As a general rule, a therapeutic indication should be a well-recognized clinical entity that is clearly distinguishable from other conditions…

They also echo Beck in warning of over-diagnosis and over-medicalization:

Current proposals to reclassify some conditions that were subthreshold or prodromal as distinct syndromes or disorders could have implications for clinical trials. The inclusion of milder or very early cases of psychiatric disorders may lead to an increase in the number of non-disordered (false-positive) patients in clinical trials, and to an increase in the placebo effect, as less severe cases are more likely to respond to placebo. It may therefore be difficult to show a statistically significant difference [of drug over placebo]…

This raises another highly controversial issue: the risk of medicalization of the normal population. In this respect, a strong concern comes from the proposal to remove bereavement exclusion from the criteria for major depressive disorder, implying that all individuals with ‘normal grief’ might be considered as patients in the future.

Regular readers will remember that I’ve covered both overdiagnosis screwing up clinical trials, and the bereavement debate.

Two and a half years ago, shortly after the first draft of the DSM-5 was made public, I predicted that the eventual release of DSM-5 would be a non-event because, by then, it would have been widely debated and criticized, destroying the illusion of expert consensus that any such document must have in order to succeed.

I think events have borne this out. An awful lot of professionals, patients, and their relatives, will reject the changes in favour of sticking with the DSM-IV or other criteria. Without swift and general acceptance, a document like the DSM is just paper. It seems increasingly likely that the DSM-5 is going to be dead on arrival.

Starcevic V, Portman ME, & Beck AT (2012). Generalized anxiety disorder: between neglect and an epidemic. The Journal of nervous and mental disease, 200 (8), 664-7 PMID: 22850300

Florence Butlen-Ducuing et al (2012). DSM‑5 and clinical trials in psychiatry: challenges to come? Nature Reviews: Drug DiscoveryDOI: 10.1038/nrd3811

Retrieved from: http://neuroskeptic.blogspot.co.uk/2012/08/dsm-5-rip.html

Sensory Integration Therapy ineffective for Treatment of Autism, Study Finds

In Autism Spectrum Disorders, General Psychology, School Psychology on Wednesday, 21 November 2012 at 14:35

Sensory Integration Therapy ineffective for Treatment of Autism, Study Finds

By: Pasha Bahsoun

Parents of children with autism are faced with many options when it comes to therapy and education for their children, from applied behavior analysis (ABA) to floortime. A new study out of the University of Texas at Austin has found that one form of therapy, sensory integration therapy, is ineffective for the treatment of autism.

Many children on the autism spectrum experience sensitivities towards sensory stimuli such as sounds, light and touch. Those who practice sensory integration therapy seek to offer children small amounts of sensory input with the goal of improving how their nervous system reacts to certain stimuli. This is accomplished through objects such as weighted blankets, weighted vests and swings.

The researchers evaluated 25 studies on sensory integration therapy and found that there was no scientific evidence that symptoms of autism were improved. Three of the studies suggested that the treatment was effective and 14 studies reported no benefits. They went further to indicate that several of the studies, including the three studies reporting positive results, had serious methodological flaws. Therefore, based on this evaluation, they were not able to support sensory integration therapy for the treatment of children with autism.

The researchers noted that sensory integration therapy may even exacerbate the symptoms of autism because it provides reinforcement for unwanted behaviors by providing access to desirable activities, like bouncing on balls, and being allowed to escape tasks like homework. In addition, children who receive this form of therapy are oftentimes also receiving other behavioral interventions simultaneously, which would undermine their effectiveness.

Agencies providing services for children with autism, as well as insurance companies, are now mandating that only evidence and research-based practices be used in interventions, which at the moment is only applied behavior analysis.

If you enjoy my articles, you can follow me on Twitter:@ThePashaB.

Retrieved from: http://www.examiner.com/article/sensory-integration-therapy-ineffective-for-treatment-of-autism-study-finds

***

Sensory Integration Treatment for Autism Spectrum Disorders: A Systematic Review

Abstract

Intervention studies involving the use of sensory integration therapy (SIT) were systematically identified and analyzed. Twenty-five studies were described in terms of: (a) participant characteristics, (b) assessments used to identify sensory deficits or behavioral functions, (c) dependent variables, (d) intervention procedures, (e) intervention outcomes, and (f) certainty of evidence. Overall, 3 of the reviewed studies suggested that SIT was effective, 8 studies found mixed results, and 14 studies reported no benefits related to SIT. Many of the reviewed studies, including the 3 studies reporting positive results, had serious methodological flaws. Therefore, the current evidence-base does not support the use of SIT in the education and treatment of children with autism spectrum disorders (ASD). Practitioners and agencies serving children with ASD that endeavor, or are mandated, to use research-based, or scientifically-based, interventions should not use SIT outside of carefully controlled research.

Highlights

► Research involving sensory integration therapy to autism was reviewed. ► Out of 25 studies, three studies had positive results. ► Serious methodological flaws were found across studies. ► The evidence-base does not support the use of SIT in the treatment of autism.

Retrieved from: http://www.sciencedirect.com/science/article/pii/S1750946712000074

%d bloggers like this: