Pub Date : 2008-10-01DOI: 10.1521/CAPN.2008.13.5.1
R. Mayes, Catherine L. Bagwell, Jennifer L. Erkulwater
Attention Deficit Hyperactivity Disorder (ADHD) holds the distinction of being both the most extensively studied pediatric mental disorder and one of the most controversial. This is partly due to the fact that it is also the most commonly diagnosed mental disorder among minors. On average, one in every ten to 15 children in the U.S. has been diagnosed with the disorder and one in every 20 to 25 uses a stimulant medication—often Ritalin, Adderall, or Concerta—as treatment. The biggest increase in youth diagnosed with ADHD and prescribed a stimulant drug occurred during the 1990s, when the prevalence of physician visits for stimulant pharmacotherapy increased five-fold. This unprecedented increase in U.S. children using psychotropic medication triggered an intense public debate.
{"title":"Medicating Children: The Enduring Controversy over ADHD and Pediatric Stimulant Pharmacotherapy","authors":"R. Mayes, Catherine L. Bagwell, Jennifer L. Erkulwater","doi":"10.1521/CAPN.2008.13.5.1","DOIUrl":"https://doi.org/10.1521/CAPN.2008.13.5.1","url":null,"abstract":"Attention Deficit Hyperactivity Disorder (ADHD) holds the distinction of being both the most extensively studied pediatric mental disorder and one of the most controversial. This is partly due to the fact that it is also the most commonly diagnosed mental disorder among minors. On average, one in every ten to 15 children in the U.S. has been diagnosed with the disorder and one in every 20 to 25 uses a stimulant medication—often Ritalin, Adderall, or Concerta—as treatment. The biggest increase in youth diagnosed with ADHD and prescribed a stimulant drug occurred during the 1990s, when the prevalence of physician visits for stimulant pharmacotherapy increased five-fold. This unprecedented increase in U.S. children using psychotropic medication triggered an intense public debate.","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"13 1","pages":"1-5, 9"},"PeriodicalIF":0.0,"publicationDate":"2008-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2008.13.5.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-10-01DOI: 10.1521/CAPN.2008.13.5.6
N. Akhtar, A. Khan
Pharmacokinetics Bupropion is a racemic mixture. The pharmacologic activity and pharmacokinetics of the individual enantiomers have not been studied. Bupropion follows biphasic pharmacokinetics best described by a 2-compartment model. The terminal phase has a mean half-life of about 21 hours, while the distribution phase has a mean half-life of three to four hours. Absorption: Bupropion has not been administered intravenously to humans; therefore, the absolute bioavailability in humans has not been determined. Following oral administration of bupropion to healthy volunteers, peak plasma concentrations of bupropion are achieved within three hours. At steady state, the mean peak concentration (Cmax) following a 150mg dose every 12 hours is 136ng/ml. In a single-dose study, food increased the Cmax of bupropion by 11% and the extent of absorption as defined by area under the plasma concentration (AUC) by 17%. Distribution: Bupropion is 84% bound to plasma proteins at concentrations up to 200mcg/ml. The extent of protein binding of the hydoxybupropion metabolite is similar to that for bupropion, whereas the extent of protein binding of the threohydrobupropion metabolite is about half that seen with bupropion. The volume of distribution (Vss/F) estimated from a single 150mg dose given to 17 subjects is 1,950L (20% CV). Metabolism: Bupropion is metabolized by CYP 2B and CYP 3A4 systems into three active metabolites, hydroxybupropion, threohydrobupropion and erythohydrobupropion. The potency and toxicity of the metabolites relative to bupropion have not been fully characterized. However, it has been demonstrated in an antidepressant screening test in mice that hydroxybupropion is one half as potent as bupropion, while threohydrobupropion and erythohydrobupropion are 5-fold less potent than bupropion. Excretion: The mean apparent clearance (Cl/F) estimated from 2 single-dose (150mg) studies are 135 (+/-20%) and 209L/hr (+/-21%). Following chronic dosing of 150mg of bupropion every 12 hours for 14 days (n=34), the mean Cl/F at steady state was 160L/hr (+/-23%). The mean elimination half-life of bupropion estimated from a series of studies is approximately 21 hours. Estimates of half-lives of metablites determined from a multiple-dose study were 20 hours for hydroxybupropion, 37 hours for threohydrobupropion and 33 hours for erythrobupropion. Following oral administration of 200mg of 14C-bupropion in humans, 87% and 10% of a radioactive dose was recovered in the urine and feces, respectively. The fraction of the oral dose of bupropion excreted unchanged was only 0.5%.
{"title":"Prescriptions Into Practice: Bupropion","authors":"N. Akhtar, A. Khan","doi":"10.1521/CAPN.2008.13.5.6","DOIUrl":"https://doi.org/10.1521/CAPN.2008.13.5.6","url":null,"abstract":"Pharmacokinetics Bupropion is a racemic mixture. The pharmacologic activity and pharmacokinetics of the individual enantiomers have not been studied. Bupropion follows biphasic pharmacokinetics best described by a 2-compartment model. The terminal phase has a mean half-life of about 21 hours, while the distribution phase has a mean half-life of three to four hours. Absorption: Bupropion has not been administered intravenously to humans; therefore, the absolute bioavailability in humans has not been determined. Following oral administration of bupropion to healthy volunteers, peak plasma concentrations of bupropion are achieved within three hours. At steady state, the mean peak concentration (Cmax) following a 150mg dose every 12 hours is 136ng/ml. In a single-dose study, food increased the Cmax of bupropion by 11% and the extent of absorption as defined by area under the plasma concentration (AUC) by 17%. Distribution: Bupropion is 84% bound to plasma proteins at concentrations up to 200mcg/ml. The extent of protein binding of the hydoxybupropion metabolite is similar to that for bupropion, whereas the extent of protein binding of the threohydrobupropion metabolite is about half that seen with bupropion. The volume of distribution (Vss/F) estimated from a single 150mg dose given to 17 subjects is 1,950L (20% CV). Metabolism: Bupropion is metabolized by CYP 2B and CYP 3A4 systems into three active metabolites, hydroxybupropion, threohydrobupropion and erythohydrobupropion. The potency and toxicity of the metabolites relative to bupropion have not been fully characterized. However, it has been demonstrated in an antidepressant screening test in mice that hydroxybupropion is one half as potent as bupropion, while threohydrobupropion and erythohydrobupropion are 5-fold less potent than bupropion. Excretion: The mean apparent clearance (Cl/F) estimated from 2 single-dose (150mg) studies are 135 (+/-20%) and 209L/hr (+/-21%). Following chronic dosing of 150mg of bupropion every 12 hours for 14 days (n=34), the mean Cl/F at steady state was 160L/hr (+/-23%). The mean elimination half-life of bupropion estimated from a series of studies is approximately 21 hours. Estimates of half-lives of metablites determined from a multiple-dose study were 20 hours for hydroxybupropion, 37 hours for threohydrobupropion and 33 hours for erythrobupropion. Following oral administration of 200mg of 14C-bupropion in humans, 87% and 10% of a radioactive dose was recovered in the urine and feces, respectively. The fraction of the oral dose of bupropion excreted unchanged was only 0.5%.","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"10 1","pages":"6-9"},"PeriodicalIF":0.0,"publicationDate":"2008-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2008.13.5.6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-08-01DOI: 10.1521/CAPN.2008.13.4.1
K. Domschke
Major Depressive Disorder (MDD) is a highly disabling disease characterized by a lifetime prevalence of 5%–25%, with women being affected approximately twice as often as men. Family and twin studies indicate a strong genetic contribution to the pathogenesis of MDD with an estimated heritability of 40%–50%. Antidepressive pharmacotherapeutic agents such as tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors (SSRI), norepinephrine and serotonin reuptake inhibitors (SNRI) or noradrenergic and specific serotonergic antidepressants (NaSSA) have proven to be highly effective for a large proportion of patients in the treatment of major depression. However, two major issues need to be addressed in the pharmacotherapy of MDD, treatment resistance and treatment intolerance. Treatment Resistance A full 30%–40% of all patients fail to respond sufficiently to initial pharmacotherapy treatment. Since it can take several weeks after treatment initiation for these agents to exert antidepressant effects, patients might have to endure this period of time without symptom relief before the antidepressant is known to be ineffective. Thus, it would be highly beneficial for providers to be able to identify non–responders to a
{"title":"Pharmacogenetics—A Useful Tool in Antidepressant Pharmacotherapy?","authors":"K. Domschke","doi":"10.1521/CAPN.2008.13.4.1","DOIUrl":"https://doi.org/10.1521/CAPN.2008.13.4.1","url":null,"abstract":"Major Depressive Disorder (MDD) is a highly disabling disease characterized by a lifetime prevalence of 5%–25%, with women being affected approximately twice as often as men. Family and twin studies indicate a strong genetic contribution to the pathogenesis of MDD with an estimated heritability of 40%–50%. Antidepressive pharmacotherapeutic agents such as tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors (SSRI), norepinephrine and serotonin reuptake inhibitors (SNRI) or noradrenergic and specific serotonergic antidepressants (NaSSA) have proven to be highly effective for a large proportion of patients in the treatment of major depression. However, two major issues need to be addressed in the pharmacotherapy of MDD, treatment resistance and treatment intolerance. Treatment Resistance A full 30%–40% of all patients fail to respond sufficiently to initial pharmacotherapy treatment. Since it can take several weeks after treatment initiation for these agents to exert antidepressant effects, patients might have to endure this period of time without symptom relief before the antidepressant is known to be ineffective. Thus, it would be highly beneficial for providers to be able to identify non–responders to a","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"13 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2008-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2008.13.4.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-07-23DOI: 10.1521/CAPN.2008.13.1.1
A. Charach
After 12 months of use, children with ADHD take their medication only 50% to 75% of the time, a proportion that decreases to less than 50% after three years of use. The Multimodal Treatment Study of ADHD documented that poor adherence to medication contributed to symptom recurrence. Over two years of use, children with ADHD who discontinued medication treatment deteriorated in comparison to those who continued use. Likewise, clinical treatment guidelines recommend that physicians pay close attention to medication adherence, noting that poor treatment adherence may contribute to treatment non–response. Though clinicians have developed strategies to address the problem of adherence among children with ADHD, few studies have investigated what contributes to early discontinuation of medications among children and adolescents with ADHD. In order to better understand the problem of treatment non–compliance, this article will apply four empirically based theoretical models of health behavior to the treatment adherence literature for children who take stimulants for ADHD. It is expected that clinicians can use the application of various models to better appreciate the complexities of treatment adherence in the care of children with ADHD.
{"title":"Stimulant Medication Adherence—Theoretical Perspectives","authors":"A. Charach","doi":"10.1521/CAPN.2008.13.1.1","DOIUrl":"https://doi.org/10.1521/CAPN.2008.13.1.1","url":null,"abstract":"After 12 months of use, children with ADHD take their medication only 50% to 75% of the time, a proportion that decreases to less than 50% after three years of use. The Multimodal Treatment Study of ADHD documented that poor adherence to medication contributed to symptom recurrence. Over two years of use, children with ADHD who discontinued medication treatment deteriorated in comparison to those who continued use. Likewise, clinical treatment guidelines recommend that physicians pay close attention to medication adherence, noting that poor treatment adherence may contribute to treatment non–response. Though clinicians have developed strategies to address the problem of adherence among children with ADHD, few studies have investigated what contributes to early discontinuation of medications among children and adolescents with ADHD. In order to better understand the problem of treatment non–compliance, this article will apply four empirically based theoretical models of health behavior to the treatment adherence literature for children who take stimulants for ADHD. It is expected that clinicians can use the application of various models to better appreciate the complexities of treatment adherence in the care of children with ADHD.","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"13 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2008-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2008.13.1.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-07-23DOI: 10.1521/CAPN.2008.13.1.5
R. Gearing, Irfan A Mian, A. Charach
ness–career model specifically focuses on these factors and the ways in which they affect seeking and accepting help in health care. These theoretical models offer concepts that can help practitioners understand family and child medication adherence behavior. Overall, practitioners need to keep in mind that parental beliefs and attitudes can strongly influence the treatment decisions that they make on their child’s behalf, that these attitudes and beliefs may change over time, and that they are shaped by a variety of social, cultural and environmental factors.
{"title":"Promoting Adherence with Children and Adolescents with Psychosis","authors":"R. Gearing, Irfan A Mian, A. Charach","doi":"10.1521/CAPN.2008.13.1.5","DOIUrl":"https://doi.org/10.1521/CAPN.2008.13.1.5","url":null,"abstract":"ness–career model specifically focuses on these factors and the ways in which they affect seeking and accepting help in health care. These theoretical models offer concepts that can help practitioners understand family and child medication adherence behavior. Overall, practitioners need to keep in mind that parental beliefs and attitudes can strongly influence the treatment decisions that they make on their child’s behalf, that these attitudes and beliefs may change over time, and that they are shaped by a variety of social, cultural and environmental factors.","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"13 1","pages":"5-9"},"PeriodicalIF":0.0,"publicationDate":"2008-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2008.13.1.5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-06-01DOI: 10.1521/CAPN.2008.13.3.1
V. Gabbay, Lev Gottlieb, D. Shungu
{"title":"1H MRS: What the Practicing Clinician Needs to Know","authors":"V. Gabbay, Lev Gottlieb, D. Shungu","doi":"10.1521/CAPN.2008.13.3.1","DOIUrl":"https://doi.org/10.1521/CAPN.2008.13.3.1","url":null,"abstract":"","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"13 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2008.13.3.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2007-12-01DOI: 10.1521/CAPN.2007.12.6.8
N. Akhtar
Guanfacine is an oral, centrally acting, alpha2–adrenergic receptor agonist used alone or in combination with other drugs for the treatment of essential hypertension. This medication works by producing a decrease in sympathetic outflow, resulting in a reduction of peripheral vascular resistance, renal vascular resistance, heart rate and blood pressure. Intuniv(Guanfacine), a non–stimulant selective alpha–2A–receptor agonist has been studied in children and adolescents with ADHD and has been considered for approval by FDA in June 2007. It binds selectively to alpha 2A adrenergic cell receptors located in the prefrontal cortex. The prefrontal cortex is an area of the brain associated with executive functioning, that is, working memory, behavioral inhibition, regulation of attention, distractibility, impulsivity, frustration tolerance, etc. The selective alpha–2A agonist strengthens working memory and prefrontal cortex neuronal firing. This research supports the use of guafacine for the treatment of ADHD.
{"title":"Prescriptions Into Practice: Guanfacine","authors":"N. Akhtar","doi":"10.1521/CAPN.2007.12.6.8","DOIUrl":"https://doi.org/10.1521/CAPN.2007.12.6.8","url":null,"abstract":"Guanfacine is an oral, centrally acting, alpha2–adrenergic receptor agonist used alone or in combination with other drugs for the treatment of essential hypertension. This medication works by producing a decrease in sympathetic outflow, resulting in a reduction of peripheral vascular resistance, renal vascular resistance, heart rate and blood pressure. Intuniv(Guanfacine), a non–stimulant selective alpha–2A–receptor agonist has been studied in children and adolescents with ADHD and has been considered for approval by FDA in June 2007. It binds selectively to alpha 2A adrenergic cell receptors located in the prefrontal cortex. The prefrontal cortex is an area of the brain associated with executive functioning, that is, working memory, behavioral inhibition, regulation of attention, distractibility, impulsivity, frustration tolerance, etc. The selective alpha–2A agonist strengthens working memory and prefrontal cortex neuronal firing. This research supports the use of guafacine for the treatment of ADHD.","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"12 1","pages":"8-10"},"PeriodicalIF":0.0,"publicationDate":"2007-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2007.12.6.8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2007-12-01DOI: 10.1521/CAPN.2007.12.6.1
M. Stein, M. Weiss, B. Leventhal
It is now well established that impairments associated with ADHD often extend beyond the school day. As a result, new treatments have been developed to improve attention and reduce overactivity and impulsivity for increasingly longer periods of time. These longer–acting methylphenidate and amphetamine–based stimulants have become the most common ADHD medications. However, in addition to their salutary effects, ADHD medications can lead to less desirable effects in other functional domains, such as sleep. This review will describe the relationship between ADHD, stimulant medication, and sleep while highlighting clinical implications. A wide variety of sleep problems often co–occur with ADHD and often may antedate treatment. In fact, treatment of some sleep disorders (e.g., Sleep Disordered Breathing Disorder, Delayed Sleep Phase Disorder) may, in and of themselves, lead to improved attention or behavior. As a result, a sleep history and baseline measure of sleep functioning are an essential component of a proper evaluation of individuals presenting with symptoms of ADHD. If a primary sleep disorder is suspected, further sleep evaluation should be conducted by appropriately trained professionals. More commonly, however, sleep problems coexist with ADHD and psychiatric comorbidity, or may result from, or are exacerbated by, stimulant medication.
{"title":"ADHD By Night: Sleep Problems and ADHD Medications","authors":"M. Stein, M. Weiss, B. Leventhal","doi":"10.1521/CAPN.2007.12.6.1","DOIUrl":"https://doi.org/10.1521/CAPN.2007.12.6.1","url":null,"abstract":"It is now well established that impairments associated with ADHD often extend beyond the school day. As a result, new treatments have been developed to improve attention and reduce overactivity and impulsivity for increasingly longer periods of time. These longer–acting methylphenidate and amphetamine–based stimulants have become the most common ADHD medications. However, in addition to their salutary effects, ADHD medications can lead to less desirable effects in other functional domains, such as sleep. This review will describe the relationship between ADHD, stimulant medication, and sleep while highlighting clinical implications. A wide variety of sleep problems often co–occur with ADHD and often may antedate treatment. In fact, treatment of some sleep disorders (e.g., Sleep Disordered Breathing Disorder, Delayed Sleep Phase Disorder) may, in and of themselves, lead to improved attention or behavior. As a result, a sleep history and baseline measure of sleep functioning are an essential component of a proper evaluation of individuals presenting with symptoms of ADHD. If a primary sleep disorder is suspected, further sleep evaluation should be conducted by appropriately trained professionals. More commonly, however, sleep problems coexist with ADHD and psychiatric comorbidity, or may result from, or are exacerbated by, stimulant medication.","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"12 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2007-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2007.12.6.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2007-10-29DOI: 10.1521/CAPN.2007.12.3.6
S. Sundram
M., Clevenger, W., Wu, M., Arnold, L. et al. (2001). Impairment and Deportment Responses to Different Methylphenidate Doses in Children With ADHD: The MTA Titration Trial. Journal of the American Academy of Child and Adolescent Psychiatry, 40(2), 180–187. Kollins, S., Greenhill, L., Swanson, J., Wigal, S., Abikoff, H., McCracken, J., Riddle, M., et al. (2006). Rationale, Design, and Methods of the Preschool ADHD Treatment Study (PATS). Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1275–1283. McGough, J., McCracken, J., Swanson, J., Riddle, M., Kollins, S., Greenhill, L., Abikoff, H., et al. (2006). Pharmacogenetics of Methylphenidate Response in Preschoolers with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1314–1322. Swanson, J., Greenhill, L., Wigal, T., Kollins, S., Stehli, A., Davies, M., Chuang, S. et al. (2006). Stimulant–Related Reductions of Growth Rates in the PATS. Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1304–1313. Wigal, T., Greenhill, L., Chuang, S., McGough, J., Vitiello, B., Skrobala, A., Swanson, J. et al. (2006). Safety and Tolerability of Methylphenidate in Preschool Children with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1294–1303.
{"title":"The Influence of Cannabis on the Developing Brain","authors":"S. Sundram","doi":"10.1521/CAPN.2007.12.3.6","DOIUrl":"https://doi.org/10.1521/CAPN.2007.12.3.6","url":null,"abstract":"M., Clevenger, W., Wu, M., Arnold, L. et al. (2001). Impairment and Deportment Responses to Different Methylphenidate Doses in Children With ADHD: The MTA Titration Trial. Journal of the American Academy of Child and Adolescent Psychiatry, 40(2), 180–187. Kollins, S., Greenhill, L., Swanson, J., Wigal, S., Abikoff, H., McCracken, J., Riddle, M., et al. (2006). Rationale, Design, and Methods of the Preschool ADHD Treatment Study (PATS). Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1275–1283. McGough, J., McCracken, J., Swanson, J., Riddle, M., Kollins, S., Greenhill, L., Abikoff, H., et al. (2006). Pharmacogenetics of Methylphenidate Response in Preschoolers with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1314–1322. Swanson, J., Greenhill, L., Wigal, T., Kollins, S., Stehli, A., Davies, M., Chuang, S. et al. (2006). Stimulant–Related Reductions of Growth Rates in the PATS. Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1304–1313. Wigal, T., Greenhill, L., Chuang, S., McGough, J., Vitiello, B., Skrobala, A., Swanson, J. et al. (2006). Safety and Tolerability of Methylphenidate in Preschool Children with ADHD. Journal of the American Academy of Child and Adolescent Psychiatry, 45(11), 1294–1303.","PeriodicalId":89750,"journal":{"name":"Child & adolescent psychopharmacology news","volume":"12 1","pages":"6-9"},"PeriodicalIF":0.0,"publicationDate":"2007-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1521/CAPN.2007.12.3.6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67088192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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