ABSTRACT
OBJECTIVE: Student-run clinics are increasingly common in medical schools across the United States and may provide new opportunities for psychiatric education. This study investigates the educational impact of a novel behavioral health program focused on depressive disorders at a student-run clinic. METHOD: The program was assessed through chart review and student self-report questionnaire. RESULTS: The rates at which students were able to diagnose and offer treatment for major depressive disorder doubled after implementation of the behavioral health program. Of the students who completed the questionnaire (N=63), nearly all (98%) agreed that their clinic experience was a valuable supplement to their psychiatric education, and 83% agreed that it taught them a skill or attitude their formal curriculum could not have. CONCLUSION: This study adds to the growing literature on student-run clinics as unique contributors to medical training by demonstrating benefits specific to psychiatric education.
Subject(s)
Clinical Competence , Depressive Disorder, Major/diagnosis , Mental Health Services/organization & administration , Psychiatry/education , Students, Medical , Ambulatory Care Facilities/organization & administration , Curriculum , Depressive Disorder, Major/therapy , Education, Medical, Undergraduate/methods , Humans , Retrospective Studies , Surveys and QuestionnairesABSTRACT
BACKGROUND: : There is paucity of knowledge on the long-term outcome of hypochondriasis, with even less knowledge about the effect of treatment with a selective serotonin reuptake inhibitor (SSRI). METHODS: : This prospective follow-up study included 58 patients with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) hypochondriasis who had participated in a trial of SSRI treatment 4 to 16 years earlier (mean ± SD = 8.6 ± 4.5 years). RESULTS: : Information was obtained on 79.3% (n = 46) of the original group. At follow-up, 40% of the patients continued to meet full DSM-IV criteria for hypochondriasis. Persistence of hypochondriasis was individually predicted by longer duration of prior hypochondriasis (P = 0.003), history of childhood physical punishment (P = 0.01), and less usage of SSRIs during the interval period (P = 0.02). Remission status was not significantly predicted by demographic characteristics, baseline hypochondriasis severity, or psychiatric comorbidity. CONCLUSIONS: : A substantial proportion of patients with hypochondriasis who receive treatment with SSRIs achieve remission over the long term. Interim SSRI use may be a factor contributing to better prognosis.
Subject(s)
Child Abuse/statistics & numerical data , Fluoxetine/therapeutic use , Fluvoxamine/therapeutic use , Hypochondriasis/drug therapy , Selective Serotonin Reuptake Inhibitors/therapeutic use , Adolescent , Adult , Aged , Clinical Trials as Topic , Diagnostic and Statistical Manual of Mental Disorders , Female , Follow-Up Studies , Humans , Hypochondriasis/diagnosis , Male , Middle Aged , Personality Disorders/complications , Personality Disorders/drug therapy , Remission Induction , Severity of Illness IndexABSTRACT
The peripheral benzodiazepine receptor (PBR) is expressed on the outer mitochondrial membrane of activated microglia and is implicated in the pathophysiology of a variety of central nervous system and peripheral diseases. The abundant receptor concentration makes PBR a potential biomarker and an attractive target for quantification in vivo using positron emission tomography. PBR can be an important target for monitoring disease progression, for evaluating the effect of therapy, and for investigating new treatment modalities. PBR is also emerging as a potential target in the treatment of neuroinflammatory and neuropsychiatric disorders. Here, we review the positron emission tomography radioligands employed for imaging PBR in living brain and their applications.
Subject(s)
Brain/metabolism , Microglia/metabolism , Positron-Emission Tomography , Radioisotopes , Radiopharmaceuticals , Receptors, GABA-A/metabolism , Animals , Brain/diagnostic imaging , Humans , Microglia/diagnostic imaging , Radioisotopes/pharmacokinetics , Radiopharmaceuticals/pharmacokinetics , RatsABSTRACT
Lyme disease, caused by the bacterium Borrelia burgdorferi, can cause multi-systemic signs and symptoms, including peripheral and central nervous system disease. This review examines the evidence for and mechanisms of inflammation in neurologic Lyme disease, with a specific focus on the central nervous system, drawing upon human studies and controlled research with experimentally infected rhesus monkeys. Directions for future human research are suggested that may help to clarify the role of inflammation as a mediator of the chronic persistent symptoms experienced by some patients despite antibiotic treatment for neurologic Lyme disease.
