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This chapter focuses on people who have memory problems resulting from a neurological condition such as traumatic head injury, stroke, encephalitis, and hypoxic brain damage. Topics discussed include the meaning of recovery, factors affecting recovery, mechanisms of recovery, how much recovery takes place, improving natural recovery, and whether treatment is effective in helping people with memory and learning difficulties.

Students with specific learning disorder (SLD) account for 35% of all students receiving special education services. In the DSM-5, SLD combines four previous diagnoses into one. The Individuals with Disabilities Education Act (IDEA) and the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) agree that children should be excluded from being diagnosed if the disorder is primarily due to environmental, cultural, or economic disadvantage. They differ on the DSM-5’s exclusion for the lack of proficiency in the language of instruction. Schools can screen for SLD using the testing or the dual-discrepancy model of response to intervention (RTI). Assessment requires a comprehensive evaluation by the school. Students with SLD often suffer from poor social skills and low self-esteem. Intervention may be titrated according to the student’s level of need using multitiered systems of support. Collaborating with teachers, parents, and community providers is especially important for these students. A case example illustrates how an ecological approach can help students grow and learn.

Given that deficits in executive functions (EF) and writing impairments are both characteristics of several neurodevelopmental disorders, this chapter explored how EF are related to writing performance in students with autism spectrum disorders (ASD), attention deficit/hyperactivity disorders (ADHD), and specific learning disorders (i.e. dyslexia and dysgraphia). Although these neurodevelopmental disorders share similar features of executive dysfunction, the profiles between groups appear to differ, and different disorders have unique executive profiles. As these unique executive profiles have an impact on successful writing, it was intended to contribute to our understanding about the cognitive mechanisms (related with EF) that underlie writing development. Also, potential implications for clinical practice were discussed.

Velo-cardio-facial syndrome (VCFS) is caused by an interstitial deletion from chromosome 22 at the 22q11 band. It is the most common microdeletion syndrome yet identified in humans, with a population prevalence of approximately 1 in 2,000 (Robin & Shprintzen, 2005). Velo-cardio-facial syndrome is known by a number of other names based on other reports in the literature that described individual components of the syndrome from a number of different perspectives. These include: DiGeorge syndrome, 22q11.2 deletion syndrome, Sedlačková syndrome, conotruncal anomalies face syndrome, and Cayler syndrome (Robin & Shprintzen, 2005). Structural anomalies affect nearly every part and system of the body and may include congenital heart disease, palatal defects, thymic hypoplasia, and endocrine disorders (Robin & Shprintzen, 2005). Velo-cardio-facial syndrome is the most common genetic cause of conotruncal heart anomalies and the most common genetic cause of cleft palate (Shprintzen et al., 2005) in addition to being the most significant genetic cause of mental illness yet identified. The earliest cases of VCFS to appear in the medical literature were probably those reported by Sedlačková in 1955 (E. Sedlačková, 1955). Sedlačková proposed a mechanism of neurologic and developmental anomalies that caused abnormalities of the palate leading to hypernasal speech and lack of facial animation caused by abnormal neurologic innervation (E. Sedlačková, 1967). The same disorder was described in 1968 by DiGeorge (DiGeorge, 1968) and by Kretschmer (Kretschmer, Say, Brown, & Rosen, 1968) who described endocrine and immunologic disorders associated with congenital heart disease. The 1st person, however, to delineate this disorder as a genetic syndrome was Strong (Strong, 1968), with his description of a single family with an affected mother and 3 affected children. Larger numbers of cases with broader phenotypic descriptions and multiple familial cases with a clear autosomal dominant pattern of inheritance followed (Shprintzen et al., 1978; Shprintzen, Goldberg, Young, & Wolford, 1981; Williams, Shprintzen, & Goldberg, 1985) thereby confirming that VCFS was a genetic syndrome. In the years that followed, the phenotypic spectrum of VCFS was expanded in a small series of papers.

Noonan syndrome (NS) is a genetic disorder characterized by short stature, typical facial dysmorphology, and congenital heart defects. Noonan syndrome may occur on a sporadic basis or in a pattern consistent with autosomal dominant inheritance, with a predominance of maternal transmission (Noonan 1994). In approximately 50% of the patients with definite NS, a missense mutation is found in the PTPN11 gene on chromosome 12. PTPN11 is one of the genes of the Ras-MAPK pathway, a signal transduction cascade that has been studied extensively for its role in human oncogenesis. The signaling cascade regulates cell proliferation, differentiation, and survival. PTPN11 encodes the nonreceptor protein tyrosine phosphatase SHP-2. The mutations associated with NS result in a gain of function of SHP-2 (Tartaglia and Gelb 2005). Recently, activating mutations in other genes of the Ras-MAPK pathway (SOS1, KRAS, RAF1) were found as the causative dominant mutations in NS. These findings establish hyperactive Ras as a cause of the developmental abnormalities seen in NS (Schubbert et al. 2007). The diagnosis is made on clinical grounds, by observation of key features. Establishing the diagnosis can be very difficult, especially at an older age. There is great variability in expression, and mild expression is likely to be overlooked. Improvement of the phenotype occurs with increasing age. The age-related change of facial appearance can be subtle, especially at older age. Several scoring systems have been devised to guide the diagnostic process). The most recent scoring system was developed in 1994 (Van der Burgt et al. 1994). The incidence of NS is estimated to be between 1:1,000 and 1:2,500 live births (Mendez and Opitz 1985). Further details on the various medical aspects of NS (e.g., congenital heart defects, skeletal and urethrogenital abnormalities, growth delay) can be found in Van der Burgt (2007). A number of conditions have phenotypes strikingly similar to NS. The first is Turner syndrome (45, X0), a well-known chromosomal abnormality in girls. A group of distinct syndromes with partially overlapping phenotypes also exist in which causative mutations are also found in genes of the RAS-MAPK pathway.

Many children with exceptionalities can participate successfully in group-composition activities as well as create works of their own when they are provided with proper tools and support. Accommodations and suggestions for including special learners in composition classes and programs are offered. Specific attention is given to a selection of more prevalent physical disabilities and learning disorders. The chapter also features suggestions for modeling and role-playing this type of teaching with pre-service teachers before they interact with PreK-12 students. The final chapter of this section uses the five domains of teaching and learning to discuss modifying instruction for children with special learning needs. In addition to the five domains, that chapter employs four teaching approaches to examine the suggestions found in the others chapters in this section in order to provide guidance for teachers working with children with special needs within the framework of composition lessons and activities. Finally the final chapter in this section provides a model for constructing case studies of children that pre-service teachers could use to further their understanding of the learning processes experienced the wide range of students likely to be found in school music programs.

Specific deficits in information processing in the brain are the commonest causes of academic difficulties in children with ADHD. For many children with ADHD, academic difficulty is not confined to a particular subject but occurs across several areas of study. This chapter explores learning difficulties in ADHD, including common areas of difficulty, including written expression, oral expression, and others. The chapter also discusses when problems become apparent, the causes of learning difficulty in ADHD (poor concentration, impulsivity, working memory impairment, defiance, low self-esteem, social difficulties, poor incentival motivation, auditory processing impairment, difficulties in spelling, handwriting, and organizing), as well as dyslexia and ADHD, and the gifted child with ADHD.