<p>Attention-Deficit Hyperactivity Disorder, (ADHD), is an established childhood psychiatric disorder, and it is the present diagnosis for children with major difficulties in the core symptoms; impulsiveness, attention and hyperactivity. The disorder is known to persist into adulthood and create major problems in coping with everyday life. With ADHD follows a vast variety of other conditions, which burdens the ADHD individuals even more. The major cause for the disorder is in heritage but also other possible explanations will be discussed. The main treatment for ADHD is psycho stimulants, such as methylphenidate and amphetamine. ADHD is associated with substance abuse and several articles in this essay will provide support for that. Is substance abuse in ADHD individuals a form of self-medication in order to ameliorate the symptoms or is the increased risk for substance abuse due to the stimulant medications? In this essay, I will describe what ADHD is, present what are its known causes, summarize the treatments available for ADHD, and discuss the relationships between ADHD and substance abuse.</p>

Thesis (Ph. D.)--University of Washington, 2000. / Vita. Includes bibliographical references (leaves 57-62).

Thesis (Ph.D)--Virginia Commonwealth University, 2009. / Prepared for: Dept. of Psychology. Title from title-page of electronic thesis. Bibliography: leaves 147-173.

Thesis (D. Min..)--St. Vladimir's Orthodox Theological Seminary, Crestwood, N.Y., 2008. / Abstract. Description based on microfiche version record. Includes bibliographical references (leaves 337-339).

Thesis (Psy.D.)--Rutgers University, 2009. / "Graduate Program in Clinical Psychology." Includes bibliographical references (p. 83-91).

Thesis (Ph. D.)--Virginia Commonwealth University, 2003. / Prepared for: Dept. of Psychology. Includes bibliographical references (leaves 63-75). Also available online via the Internet.

Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.

Anxiety disorders, including social anxiety disorder (SAD) and posttraumatic stress disorder (PTSD) are common and disabling conditions. Largely based on animal and pharmacological studies, both the serotonergic and substance P/neurokinin-1 (SP/NK1) systems have been implicated in their underlying pathology. However, only few neuroimaging studies have directly assessed these neurotransmitter systems in human sufferers of anxiety disorders, and none have addressed possible between-systems relationships. The overall aim of this thesis was to study possible neurochemical alterations associated with anxiety disorders. To this end, three studies using positron emission tomography (PET) for in-vivo imaging of the brain serotonergic and SP/NK1 systems in patients with SAD and PTSD were conducted. The radiotracers [11C]5-HTP, [11C]DASB, and [11C]GR205171 were used to index serotonin synthesis rate, serotonin transporter (SERT) availability, and NK1 receptor availability respectively. In Study I, patients with SAD relative to controls exhibited enhanced serotonin synthesis rate and serotonin transporter availability. Serotonin synthesis rate in the amygdala was positively related to social anxiety symptom scores. Study II demonstrated increased NK1 receptor availability in the amygdala in patients with SAD relative to controls. In Study III, patients with PTSD showed elevated NK1 receptor availability in the amygdala as compared to controls. SERT availability in the amygdala was negatively related to PTSD symptom severity, a relationship that was moderated by NK1 receptor levels. The regional overlap between SERT and NK1 receptor expression was altered in patients with PTSD, with reduced overlap linked to more severe symptoms. Collectively, the findings are consistent with the view that serotonin in the amygdala induces rather than reduces anxiety and links exaggerated anxiety to an overactive presynaptic serotonin system. In addition, the involvement of the SP/NK1 system in stress and anxiety, as suggested by animal studies, was demonstrated in two common human anxiety disorders. Finally, PTSD symptomatology is better accounted for by interactions between the serotonergic and SP/NK1 systems in the amygdala than by each system separately. In conclusion, this thesis supports that both the serotonergic and SP/NK1 systems in and of themselves, but also interactively, may be important contributors to anxiety symptomatology.

The economic burden of prescription opioid abuse is believed to be substantial, however it is not known whether total and per-event hospital (ED and inpatient) costs associated with opioid abuse or misuse differ by insurance status. We also wanted identify predictors of charges. We used the 2006, 2007, and 2008 files of the Healthcare Cost and Utilization Project's Nationwide Emergency Departments Sample (HCUP-NEDS) to identify events and charges assigned opioid abuse, dependence, or poisoning ICD-9-CM diagnosis codes (304.0X, 304.7X, 305.5X, 965.00, 965.02, 965.09). Using methods to account for the sampling design of the NEDS, we estimated national total and mean charges -- overall and by insurance status (Medicare, Medicaid, private insurance, or self-payment). Charges were adjusted using the 2010 Medical Consumer Price Hospital Services index. We used a log-linked gamma regression model to assess potential predictors of charges. The number of opioid abuse-related events was 515,896; 506,837; and 564,559 for 2006, 2007, and 2008, respectively. Approximately 55% visits in each year resulted in inpatient admissions. Total charges billed for opioid abuse-related events were US$9.8; 9.6; and 9.5 billion for 2006, 2007, and 2008, respectively. Medicaid patients had the highest charges in each years followed by Medicare patients. Approximately 93% of total charges were due to subsequent inpatient admission. Overall unadjusted mean charges were $20,651; $20,373; and $18,384 for 2006, 2007, and 2008, respectively. Compared to events paid for by private insurance, Medicaid-covered events had significantly higher mean charges, and self-paid events had significantly lower charges (p < 0.001 for each year). Inpatient admissions resulted in significantly higher mean charges compared to treat-and-release ED visits (p < 0.001 for each year). We found similar results after adjusting for clinical and demographic factors. Age, number of diagnoses, inpatient admission, presence of cardiac tissue disorders, respiratory infections or failure, gastrointestinal hemorrhage, and acute pancreatitis were significantly positively associated with total charges billed (p < 0.001 for all). This study helps in determining differences in hospital costs of opioid abusers by insurance status and in identifying potential predictors of such costs, resulting in better understanding the economic burden of opioid abuse on the healthcare system. / text

published_or_final_version / Clinical Psychology / Master / Master of Social Sciences