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Books on the topic 'H severe intellectual disability'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Avery, Jocelyn D. An Ethnography of Severe Intellectual Disability. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-32209-0.

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Gargiulo, Richard M., and Emily C. Bouck. Instructional Strategies for Students With Mild, Moderate, and Severe Intellectual Disability. 2455 Teller Road, Thousand Oaks California 91320: SAGE Publications, Inc., 2018. http://dx.doi.org/10.4135/9781506369785.

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3

Clews, Francesca. Non-governmental organisations serving people with profound intellectual disability and severe psychiatric disability: Present situation and the way forward. Johannesburg: Centre for Health Policy, University of the Witwatersrand, 1998.

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4

Butterfield, Nancy. Partners in everyday communicative exchanges: A guide to promoting interaction involving people with severe intellectual disability. Baltimore: Paul H. Brookes Pub. Co., 1995.

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5

Butterfield, Nancy. Partners in everyday communicative exchanges: A guide to promoting interaction involving people with severe intellectual disability. Sydney: MacLennan & Petty, Australia, 1995.

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6

Avery, Jocelyn D. An Ethnography of Severe Intellectual Disability: Becoming 'Dirty Little Freaks'. Palgrave Macmillan, 2019.

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7

Gargiulo, Richard M., and Emily C. Bouck. Instructional strategies for students with mild, moderate, and severe intellectual disability. 2018.

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8

Sigafoos, Jeff, Michael Arthur, and Nancy Butterfield. Partners in Everyday Communicative Exchanges: A Guide to Promoting Interaction Involving People With Severe Intellectual Disability. Brookes Publishing Company, 1996.

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9

Moss, Joanna, Patricia Howlin, and Chris Oliver. The Assessment and Presentation of Autism Spectrum Disorder and Associated Characteristics in Individuals with Severe Intellectual Disability and Genetic Syndromes. Oxford University Press, 2011. http://dx.doi.org/10.1093/oxfordhb/9780195305012.013.0018.

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10

Gregory, Mary Lee. Congenital Hypothyroidism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0058.

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Congenital hypothyroidism (CH) results from the effects of insufficient thyroid hormone on the developing fetus and infant, and is characterized by severe intellectual disability and growth inhibition. CH can result from maternal iodine deficiency, which can be abolished by appropriate dietary iodine supplementation. Alternately, CH may be caused by congenital defects of the thyroid gland and thyroid hormone biosynthesis abnormalities (primary congenital hypothyroidism), or by “central hypothyroidism,” in which the brain produces insufficient thyroid stimulating hormone. Treatment of these latter etiologies requires administration of thyroid hormone.

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11

Johnston, Michael V. Coffin-Lowry Syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0057.

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Coffin-Lowry syndrome (CLS) is a relatively rare (1:50,000-100,000 incidence) sex-linked neurodevelopmental disorder that includes severe intellectual disability, dysmorphic features including facial and digital abnormalities, growth retardation, and skeletal changes. Most cases are sporadic with only 20% to 30% of cases having an additional family member. CLS is caused by variable loss of function mutations in the RPS6KA3 gene that maps to Xp22.2 and codes for the hRSK2 S6 kinase that phosphorylates the transcription factor CREB (cAMP response element binding protein) as well as other nuclear transcription factors. Phosphorylated CREB (pCREB) plays a major role in memory formation in fruit flies and mammals by activating specific genes through epigenetic histone acetylation.

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12

Vernon, Hilary. Phenylketonuria. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0064.

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Phenylketonuria is an autosomal recessive biochemical disorder most often resulting from a deficiency of phenylalanine hydroxylase, the enzyme which catalyzes the conversion of phenylalanine to tyrosine. The remainder of the cases are caused by abnormalities in the phenylalanine hydroxylase cofactor, tetrahydrobiopterin. Phenylketonuria can be divided into three subgroups based on the elevation of plasma phenylalanine in the untreated state: “classical,” “variant,” and “benign.” Untreated individuals with classical phenylketonuria develop neurocognitive abnormalities including seizures, microcephaly, and severe intellectual disability. Other clinical effects include a musty body odor, eczema, and reduced skin pigmentation. Treatment, which includes dietary restriction of phenylalanine, supplementation with synthetic protein, and, in some cases, administration of a synthetic form of tetrahydrobiopterin, is successful in preventing the long-term consequences of phenylketonuria.

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13

Cheillan, David, and Frédéric Sedel. Disorders of Creatine Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0010.

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Creatine is a physiological guanidino compound playing a major role in energy metabolism in muscle and implicated in neurotransmission in brain. The three disorders of creatine metabolism (AGAT and GAMT deficiencies and the X-linked creatine transporter defect) are a group of inborn errors of metabolism characterized by a depletion of creatine that could be easily diagnosed by mesasurement of guanidinoacetate and creatine in body fluid or cranial MRS spectroscopy. The main clinical features of these paediatric disorders are intellectual disability and speech delay and some adult patients have been described with severe language impairment and mental retardation. Although the X-linked creatine transporter defect is currently not treatable, the clinical symptoms of the two disorders of creatine synthesis should be improved by creatine supplementation emphasizing the importance of an early diagnostic.

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14

Morava, Eva, and Mirian C. H. Janssen. Congenital Disorders of Glycosylation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0063.

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Congenital disorders of glycosylation (CDGs) are usually diagnosed during infancy or childhood with severe multisystem disorder and neurologic presentation. With the increasing number of surviving adult patients, recognition of the distinct adult phenotype and awareness of the diagnostic difficulties in adulthood is essential. Patients with O-glycosylation defects or with abnormal dolichol synthesis might present first in adulthood. The majority of cases with adult CDG have a neurologic disease with intellectual disability, ataxia, speech disorder, visual disturbance, and skeletal findings. Psychological abnormalities are also common. Thrombotic complications and endocrine dysfunction might persist to adulthood. MPI-CDG, the only treatable form of CDG, might progress to chronic liver failure. Genetic testing is recommended in suspected cases, since transferrin screening analysis can be normal in adults, even in N-linked glycosylation disorders.

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15

Robinson, Elise B., Benjamin M. Neale, and Mark J. Daly. Diagnosis and Epidemiology of Pediatric Psychiatric Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0058.

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Pediatric psychiatric conditions are rising in estimated prevalence, and these disorders place an enormous burden on parents, educators, and the health care system. This rise in prevalence likely contains elements of diagnostic changes, greater awareness of these disorders, and true changes in incidence. It has been estimated that there is nearly a 50% lifetime childhood prevalence of one or more mood, anxiety, or behavioral disorders (excluding eating and substance abuse disorders) and that more than 20% of children meet the definition of severe impairment. This chapter focuses on epidemiology, heritability, and implied genetic architecture in representative pediatric neuropsychiatric conditions. We consider five major diagnostic categories and highlight major diagnosis within each, specifically, intellectual disability, pervasive developmental disorders (autism spectrum disorder [ASD]), hyperactive and inattentive behavior (attention deficit/hyperactivity disorder [ADHD]), obsessive compulsive disorder (OCD) and tic disorders (TD) (which includes Tourette Syndrome [TS] and other chronic tic disorders).

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16

Chrzanowski, Daniel T., Elisabeth B. Guthrie, Matthew B. Perkins, and Moira A. Rynn. Child and Adolescent Psychiatry. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199326075.003.0015.

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Common disorders of children and adolescents include neurodevelopmental disorders (e.g., intellectual disability, autistic spectrum disorder, and learning disorders), internalizing disorders (e.g., mood and anxiety disorders), and externalizing disorders (e.g., oppositional defiant disorder and conduct disorder). The assessment of a child or adolescent patient always includes multiple informants, the context in which the child’s difficulties occur, and a functional behavioral assessment. Patients with autism spectrum disorder tend to have persistent deficits in social communication and social interaction, a restricted repertoire of behaviors and interests, and abnormal cognitive functioning. Children with disruptive mood dysregulation disorder experience chronic and severe irritability and frequent temper outbursts. Attention deficit hyperactivity disorder is characterized by hyperactivity, impulsivity, and inattention before 12 years of age. Behavior therapy has been effectively used to treat children and adolescents with neurodevelopmental disorders, attention deficit hyperactivity disorder, tic disorders, feeding and elimination disorders, and externalizing disorders. Fluoxetine is approved for treatment of depression in children and escitalopram, for adolescents. Methylphenidate and amphetamine preparations are first-line treatment for children with attention deficit hyperactivity disorder.

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