In developmental disabilities

Rojahn, J. (1994) Epidemiology and topographic taxonomy of self-injurious behavior. In Thompson, T. and Gray, D.B., eds. Destructive Behavior in Developmental Disabilities Diagnosis and Treatment. Thousand Oaks, CA Sage pp. 49-67. 

Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314-6399, USA e-mail cxgong mail.csi.cuny.edu... 

Sandler A (2005) Placebo effects in developmental disabilities implications for research and practice. Ment Retard Dev Disabil Res Rev 11 164-170. 

Gidal BE, Anderson GD, Rutecki PI Shaw R, Lanning A. Lack of effect of valproate concentration on lamotrigine pharmacokinetics in developmentally disabled patients with epilepsy. Epilepsy Res (2000) 42, 23-31. 

Hollway JA, Aman MG. Pharmacological treatment of sleep disturbance in developmental disabilities a review of the literature. Res Dev Disabil. 2011 32 939-962. 

New York State Institute for Basic Research in Developmental Disabilities... 

Volume 1 Analysis of reproductive outcomes and environmental exposures in Woburn, MA. Massachusetts Department of Public Health, Bureau of Environmental Health Assessment, Massachusetts of Health Research Institute in collaboration with the Division of Birth Defects and Developmental Disabilities, U.S. Centers for Disease Control and Prevention. 

Household contacts and sex partners of persons with chronic hepatitis B infection and health care and public safety workers with exposure to blood in the workplace Clients and staff of institutions for the developmentally disabled... 

P. J. Landrigan, C. B. Schechter, J. M. Lipton, M. C. Fahs, and J. Schwartz. Environmental Pollutants and Disease in American Children Estimates of Morbidity, Mortality, and Costs for Lead Poisoning, Asthma, Cancer, and Developmental Disabilities. Environmental Health Perspectives Volume 110, Number 7, July 2002... 

Ali, Z. 2001. Pica in people with intellectual disability a literature review of aetiology, epidemiology and complications. Journal of Intellectual and Developmental Disability, 26 205-215. 

This chapter is concerned with the neurochemical basis of developmental disability which is considered here in two forms the globally delayed or halted development seen in mental retardation, and the more circumscribed pattern of disordered development of autism. A range of deficits of important key aspects of consciousness are apparent in both conditions. Of particular relevance to consciousness are the cognitive and behavioural impairments in attention, concentration, memory, information processing and social behaviour which are commonly present. Consideration of aberrant neurotransmitter activities in these developmental deficits may provide insights into the role of neurotransmitters in consciousness. 

Gdlberg, C. 8c G. O Brien (Eds.) (2000). Developmental Disability Behaviour. Clinics in Developmental Medicine number 149, London Mac Keith Press. 

Lou, H.C., Henriksen, L., and Bruhn, P. (1990) Focal cerebral dysfunction in developmental learning disabilities. Lancet 335 S-11. 

An improved understanding of the neurobiological substrates underlying attentional mechanisms, as well as the mechanisms of stimulant action, could aid in the development of future medication formulations. The lack of data on stimulant use in particular populations, especially among preschoolers and children with developmental disabilities, and questions regarding the safety and efficacy of long-term stimulant treatment underscore the need for further research. 

Sovner et al. (1998) have done an excellent job summarizing the data on antidepressants in patients with developmental disabilities. There have been nine reports of antidepressant use in adults with depression and MR and three reports of antidepressant use in children and adolescents. Eight of nine reports in adults were positive. The drugs studied included nialimide (n = 27), fluoxetine (9), imipramine (6), amoxapine (2), and nortriptyline (1) (total n = 45). In addition, Sovner et al. identified four reports of antidepressant use in children. One involved successful treatment with fluoxetine in an adolescent, another indicated efficacy with imipramine and amitriptyline in 9 of 12 children (Do-sen, 1982), and a third showed successful management in 3 of 4 children treated with imipramine or tryptophan plus nicotinamide (Dosen, 1990). One study of fluoxetine in depressed children with autism and MR witnessed improvement in depression but not in compulsive symptoms (Ghaziuddin and Tsai, 1991). 

In the Expert Consensus survey, the use of the SSRIs was endorsed as the first-line treatment for a major depressive episode (Rush and Frances, 2000). The SSRIs were followed, at some distance, by venlafaxine, nefazodone, bupropion, and tricyclics, in that order. The warning against using bupropion in the presence of epilepsy constitutes a limitation on its use in the developmental disabilities. Clearly, more research is needed on the effects of antidepressants in both children and adolescents with MR and depression, as there are only four studies available thus far and that did not focus on age. 

There have been numerous trials of use of the atypical antipsychotics in patients with developmental disabilities, but most of these trials were uncontrolled open-labeled studies or case reports (Aman and Madrid, 1999). Findings were reported for 86 adults and 1 child with prominent self-injury. The reports of adults assessed clozapine (1 report) and risperidone (4 reports). Improvement was observed for a majority of participants in all of these trials. The patients presented with a multitude of conditions, ranging from nonspecific MR and associated behavior problems, to pervasive developmental disorders (including autism), to various psychiatric disorders, including schizophrenia and manic disorder. Self-injury appeared to respond to treatment regardless of concomitant condition. In the only clozapine report with a child (who had autistic disorder), a mean dose of 283 mg/day caused a transient reduction in self-injury. 

Aman, M.G. (1993) Efficacy of psychotropic drugs for reducing self-injurious behavior in the developmental disabilities. Ann Clin Psychiatry 5 171-188. 

Aman, M.G. (1996) Stimulant drugs in the developmental disabilities revisited. / Dev Phys Disabil 8 347-365. 

Aman M.G., Arnold, L.E., and Armstrong S. (1999) Review of serotonergic agents and perseverative behavior in patients with developmental disabilities. J Child Adolesc Psychopharmacol 5 279-289. 

Aman, M.G. and Madrid, A. (1999) Atypical antipsychotics in persons with developmental disabilities. Ment Retard Dev Disabil Res Rev 5 253—263. 

Arnold, L.E., Gadow, K., Pearson, D.A., and Varley, C.K. (1998) Stimulants. In Reiss, S. and Aman, M.C., eds. Psychotropic Medications and Developmental Disabilities The International Consensus Handbook. Columbus, OH The Ohio State Univetsity Ni-songer Center, pp. 229—257. 

ADHD, attention-deficit hyperactivity disorder DD, developmental disabilities DEX, dexedrine MPH, methylphenidate N, total number of subjects in entire study n, number of preschool-age subjects in study SE, side effect. 

King, B.H., Wright, M., Snape, M., and Dourish, C.T. (2001b) Case series amantadine open-label treatment of impulsive and aggressive behavior in hospitalized children with developmental disabilities. / Am Acad Child Adolesc Psychiatry 40 654—657. 

The population studied should also be appropriate to the disorder. For example, in a study of antibiotics for pneumococcal pneumonia, the subject population should have this disease and not a viral pneumonitis. The same applies for an antipsychotic, which should not be studied in populations such as chronic, treatment-resistant or agitated, developmentally disabled patients. If studying an agent thought to benefit treatment resistance, however, one might deliberately select a patient population that satisfied such criteria. 

Because the most common condition studied is schizophrenia, this is the primary disorder discussed. We also consider schizophrenic spectrum (e.g., delusional, schizophreniform, schizoaffective) mood disorders with psychotic features and various nonpsychotic conditions (e.g., in the developmentally disabled) for which antipsychotics have been used (see Appendix A Appendix C Appendix E, Appendix F. and Appendix G). 

Sandman C, Haney Copley K, Marion S, et al. Risperidone in patients with developmental disabilities reduces maladaptive and increases prosocial behavior amon adults. Presented at the 38th... 

Exposure to powerful drugs does have a serious impact on infant mortality, including low birth weight, developmental disabilities, and sudden infant death syndrome (SIDS). Use of crack cocaine has declined somewhat since the 1990s, but a 2001 study by the Journal of the American Medical Association concluded that much of the damage previously attributed to cocaine use may in fact be attributable to alcohol or tobacco that was also used by the mothers in question. Even moderate use of alcohol poses a risk to the fetus. 

Fanconi syndrome (metabolic acidosis secondary to malfunction of proximal renal tubules, resulting in urinary excretion of amino acids, glucose, phosphate, bicarbonate, uric acid, and other substances) secondary to longterm valproic acid has been described in an 8-year-old boy with severe developmental disability (1170). In a review of 10 previous reports of Fanconi syndrome secondary to long-term valproic acid therapy the authors found that all occurred at 4-14 years, all had taken valproic acid for 10 months to 10 years, and symptoms were fully reversible within 2-14 months after withdrawal of valproic acid. Most of the patients (9 of 11) were severely disabled, bedridden, or wheelchair-bound. 

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