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In Atkins v. Virginia (2002), the United States Supreme Court held that executing criminal offenders who are mentally retarded violates several provisions of the United States Constitution. This chapter discusses forensic mental health assessments conducted to determine whether criminal offenders are mentally retarded and, therefore, ineligible for the death penalty. It also closely examines how states have defined mental retardation in the wake of Atkins, and whether those definitions are consistent with accepted clinical standards. Assessing for mental retardation in capital contexts raises a variety of clinical challenges for forensic mental health professionals, including how intellectual functioning and adaptive deficits are assessed among correctional populations. In addition, this chapter discusses the procedural and substantive laws that govern Atkins-type evaluations.

This chapter examines how deprivation became an accepted etiological factor for intellectual disability, appearing in all the major classifications of the time and readily adopted by psychiatrists. It suggests that theories of deprivation helped shift the focus from the profoundly disabled to the large group of children who were diagnosed at the time with “mild mental retardation”. It also examines how theories of deprivation provided the scientific framework that enabled the diagnoses of a disproportionately large number of African American children as “mildly mentally retarded”.

In this chapter the basis and nature of genomic disorders are described with examples including DiGeorge Syndrome, Williams-Beuren syndrome, Charcot Marie Tooth disease, Prader-Willi, and Angelman syndromes. The mechanisms whereby chromosomal rearrangements may lead to genomic disorders are described, the nature of reciprocal genomic disorders involving deletion or duplication of particular genomic regions and of genomic disorders involving parent of origin effects are also described. Mechanisms leading to genomic disorders through disruption of control of gene expression are also described. Diseases arising from terminal and subtelomeric deletions are highlighted together with the occurrence of inversions in both healthy individuals and those with diseases such as haemophilia A. The application of array comparative genome hybridisation (arrayCGH) techniques to define submicroscopic structural variation responsible for mental retardation is reviewed to illustrate the clinical utility and application of this approach.

The topic of this chapter is neurodevelopmental disabilities, with discussion focused on three prototypic neurodevelopmental disorders: mental retardation, autism, and cerebral palsy. These disorders are highlighted because the epidemiologic knowledge is more advanced; however, many of the important methodologic issues apply to other neurodevelopmental disorders. The chapter discusses the particular research challenges in achieving complete case ascertainment due to the problems of case finding and case confirmation. It presents information about the prevalence of each of these disorders and temporal changes in frequency over time, as well as the possible factors contributing to increased recognition of these disorders. The chapter summarizes investigations of risk factors for each disorder, including genetic factors and possible environmental etiologies.

This chapter discusses legal cases relevant to forensic mental health professionals involved in capital cases. After providing a brief historical overview of death as a punishment, this chapter focuses on death penalty jurisprudence in the United States, with a particular focus on cases decided when the modern era of the death penalty began in 1972. The chapter discusses cases that address whether certain classes of offenders, such as those with mental retardation, are eligible for the death penalty. It also discusses cases that address the constitutional requirement that offenders be competent for execution. Although the focus of this chapter is predominantly on cases decided by the United States Supreme Court, it also discusses several influential and informative cases from lower federal and state courts.

Although intellectual disability has been recognized since antiquity, interest in its classification did not develop until the nineteenth century, when it became apparent that intellectual disability is not one homogeneous category, as was previously thought, but has many causes. Moreover, it became apparent that intervention could be beneficial and that interventions might be tailored for specific disorders. Early authors prepared the way for modern efforts to differentiate specific conditions that differ in both etiology and pathology, yet all result in intellectual disability. Some attempts were misguided. J. Langdon Hayden Down, in his ethnic classification (1866; Jordan, 2000), sought to classify based on the physical appearance of the individuals he examined. His goal was to absolve parents of self-blame for the handicap by emphasizing a constitutional basis for their child’s disorder. He proposed an “ethnic classification,” suggesting that the various forms of intellectual disability represented regressions to stereotypical racial forms (e.g., mongoloid, Aztec). Although he later abandoned this unfortunate idea, he continues to be known for it. Still, he is credited with drawing scientific attention to the syndrome bearing his name (Jordan, 2000) and for suggesting that the best classification is one based on etiology. Subsequently, he anticipated current efforts at classification by describing three major groups: (1) congenital, which included microcephalic, macrocephalic, hydrocephalic, epileptic, and paralytic types; (2) developmental, with a vulnerability to mental breakdown with stress during a developmental crisis; and (3) accidental (caused by injury or illness). Later, William Weatherspoon Ireland (1877), in his textbook on intellectual disability, suggested 10 subdivisions. Among these are genetous (congential), microcephalic, epileptic, eclamptic, hydrocephalic, paralytic, traumatic, inflammatory, cretinism, and idiocy by social and physical deprivation. In 1880, tuberous sclerosis complex was identified by Désiré-Maglione Bourneville (1880), who established that intellectual disability might result from brain pathology. Subsequently, many other intellectual disability syndromes were recognized. Thus began a new era, with investigators searching for clearly defined disorders associated with intellectual disability; these were commonly named after their discoverers. It was an era when intellectual disability syndromes were beginning to be recognized, but medicine had little to offer therapeutically.

This chapter uses the clinical entity of mental retardation to trace the paradigmatic changes occurring soon after World War II that introduced genetics into epidemiology and influenced public health practices. Four different classes of disorder, each underlying a distinctive form of mental retardation, will serve to illustrate this theme and this time. For each class the potential for primary and secondary prevention exists. Epidemiologic studies have furthered understanding of these quite different genetic phenomena.

This chapter examines how disability diagnoses and parental practices are distributed across different groups of parents and what kinds of arguments about parents' involvement can initially be made based on this distribution. The findings reveal the shift in the number of learning disability (LD) diagnoses from the privileged to the less privileged children. This chapter also considers other disabilities such as mental retardation and autism spectrum disorders and compares the diagnoses of these disabilities with that of LD.

The aim of this book is to provide professionals with the latest and most reliable information on intellectual disability and associated impairments. It utilizes a developmental perspective and reviews the various types of intellectual disability, discusses approaches to classification, diagnosis, and appropriate interventions, and provides information on resources that may offer additional help. The term “intellectual disability” is used throughout this book instead of “mental retardation” to reflect current perspectives. Intellectual disability refers to impairments in both cognitive functioning and adaptive skills whose onset is during the developmental period. It is a developmental, intellectual, and cognitive disability. Although the term “mental retardation” continues to be used in the International Classification of Diseases (ICD-10) and DSM-IVTR, the continued use of this designation has been questioned because it implies a static, unchanging condition rather than one that can change over time. Other terms, such as “mental handicap” and “learning disability,” have also been used. These variations in terminology are derived from long-standing concerns about the stigma of applying the term “mental retardation” to individuals. A more general term applied to individuals with intellectual disability is “mental disability.” The World Health Organization and the United Nations generally use the term “mental disability” as a broad descriptor, and the U.S. Supreme Court, in the Olmstead decision emphasizing the importance of community living, also used the term “mental disability.” The definition of “mental retardation” has changed nine times over the past 100 hundred years in the United States. Such changes in nomenclature come about with the acquisition of new knowledge regarding causes and efforts to preserve the dignity of persons who are intellectually disabled. Reflecting this new knowledge and concerns about the stigma sometimes associated with the term, on July 25, 2003, the name of the federal advisory committee, the President’s Committee on Mental Retardation (PCMR), was changed to the President’s Committee for People with Intellectual Disabilities (PCPID). Because the name designates the committee that advises the Secretary of Health and Human Services and the President on federal policy regarding programs and services, the change is noteworthy.

When a health care professional becomes engaged in diagnosing and treating or supporting a person with intellectual disability, the complexities of the disorder become apparent. To provide the best care and the best support, knowledge about neurogenetic syndromes, management of biomedical and behavior features, psychosocial interventions, and the natural history of the disorder are critical. Background knowledge and sensitivity to the needs and life challenges of the affected person are especially important. With new knowledge in genetics, the neurosciences, and social sciences, and the utilization of the richness of family, school, and community resources for these individuals as they develop, the historical stigma of the diagnosis can be reduced and hopefully eliminated. Professionals, families, and community support personnel must join forces so that all available resources are fully utilized, thus allowing the person with intellectual disability to be appropriately treated for his condition and to begin to make choices and become a self-advocate to the extent possible. This chapter will review changing concepts of intellectual disability over the centuries to provide a context for current diagnostic and treatment approaches. An awareness of this history provides perspective on the centuries-long struggle to recognize the needs of and to provide support to persons with intellectual disability. Legal safeguards are now in effect and are continuing to emerge as services are established that use a developmental model and emphasize a developmental perspective. This model emphasizes how comprehensive evaluation and positive supports at home and in the community can make a difference in the lives of persons with disabilities. The starting point is a definition of the term “intellectual disability.” This will be followed by a brief historical survey of origins and attitudes that are changing after centuries of stigmatization and separation. National and international efforts, which began in the 1970s, are continuing to encourage community placement of and self-determination by persons with intellectual disability. Although “mental retardation” is the term used in both the International Classification of Diseases (lCD-10) (World Health Organization, 1992) and the Diagnostic and Statistical Manual (DSM-IV, DSM-IVTR) (American Psychiatric Association, 1994, 2000) systems that describe an intellectual and adaptive cognitive disability that begins in early life during the developmental period, the preferred term is “intellectual disability” internationally, especially in English-speaking countries.

This chapter discusses the measurement of genius in Alfred Binet's “measuring scale of intelligence,” which he devised and successively refined between 1905 and 1911 (the year he died). Here, the chapter shows how experimental psychology had its own part to play in forming the basis of the child prodigy. And Binet's invention put France at the forefront of developmental psychology. In the words of the American introduction to the 1916 translation of Les Idées modernes sur les enfants, Binet's measuring scale was a “magnum opus” whose rapid acceptance worldwide was “little less than marvelous.” This invention established a language in which genius could be quantified, and precocity plotted against scientifically established developmental norms.

This chapter describes screening and diagnosis for congenital hypothyroidism (CH). CH is a well-established cause of mental retardation which can be prevented by screening and treatment with thyroxine.

This chapter examines violence and aggressive behaviour in psychiatric populations. The result indicate that two major psychoses, schizophrenia and mood disorders, can involve increased aggressive behaviour. Mental and behavioural problems originating in childhood, such as mental retardation and hyperactivity, may also include excessive aggressive behaviour. This chapter explains that intermittent explosive disorder, which includes outbursts of assaultive behaviours, has many characteristics resembling those of seizures associated with aggression. It also explores various treatment methods for brain dysfunction.

The Smith-Magenis syndrome (SMS) is a multiple congenital anomaly and mental retardation syndrome (Greenberg et al. 1996). The clinical phenotype includes distinctive craniofacial and skeletal features that change with age, a history of infantile hypotonia, significant expressive language delay, mental retardation, stereotypies, behavioral problems, and a sleep disorder (Potocki et al., 2000; De Leersynder et al. 2001). Two genetic mechanisms can cause SMS: an interstitial deletion involving chromosome 17p11.2 (including the retinoic acid–induced 1 [RAI1] gene) or a mutation in the RAI1 gene (Smith et al. 1986; Seranski et al. 2001; Slager et al. 2003). First described by Smith and colleagues in 1982, in two severely impaired patients (Smith et al. 1982), the phenotypic spectrum has been expanded by the recognition of additional cases (Smith et al. 1986; Stratton et al., 1986). The estimated prevalence of SMS deletion cases was reported to be 1 in 25,000 (Greenberg et al. 1991). However, new cases identified in the last decade as a result of improved molecular cytogenetic techniques (including microarray technology) now suggest the incidence to be closer to 1 in 15,000 births (Elsea and Girirajian 2008). Despite this improvement in technology accounting for new cases identified in the last several years, clinical diagnosis based on phenotypic recognition is often delayed. The phenotype of SMS becomes more pronounced and recognizable with advancing age both in terms of the physical and dysmorphic characteristics, as well as in the behavioral features (Gropman et al. 2006). Infants with SMS present with hypotonia, weak hoarse cry, decreased vocalization, and complacency (Gropman et al. 1998; 2006; Martin et al. 2006; Wolters et al.,2009). Gross and fine motor skill development is delayed in the first year of life. Sensory integration problems are frequently noted. Social skills are often age appropriate, delaying diagnosis in some cases. In older children, developmental delay, in particular expressive language delays, as well as emerging behavioral difficulties (Gropman et al. 2006; Martin et al. 2006; Madduri et al. 2006) and sleep disturbance may bring patients to clinical attention.

This chapter uses the history of Kew Cottages, (1887-2008), the first purpose-built institution for people with intellectual disabilities in Australia, as a lens through which to explore the history of Australian intellectual disability policy and practice. Influenced by international thinking, the broad outline of Australia’s policy history follows a similar pattern to other western countries. In the first decades of the twentieth century, in an atmosphere of anxiety about the ‘menace of the feeble-minded’, policy emphasised institutional segregation. In its last decades, policies of normalisation and deinstitutionalisation promised to return people with intellectual disabilities to the community. Yet the life stories of the Cottages’ residents recounted here reveal that in the nexus between policy and practice, the lives of people with intellectual disabilities could prove paradoxical.

The Kennedy family, though extremely keen on physical fitness, was plagued by illness and untimely death. In the years before John F. Kennedy was elected to the presidency, two of his siblings had suffered violent deaths in plane crashes, and his sister Rosemary had been institutionalized after a horribly botched lobotomy operation. Less than a year into his presidency, JFK’s father, Joseph P. Kennedy, was felled by a near-fatal and debilitating stroke that robbed him of his ability to communicate in speech or writing. During the difficult times that marked his tenure in office, the effects of these tragedies was incalculable, especially the loss of his father, upon whom he had always relied for counsel, encouragement, and reassurance. The family’s woes also played a part in Kennedy’s appointment of a presidential panel on mental retardation and in his support for a major health-care legislation.

This chapter examines psychologists’ involvement in the 1960s and 1970s in inventing a diagnosis known as “minimal brain dysfunction” (MBD) – a precursor to attention deficit attention disorder (ADHD). Although asserted to be a physiological matter, one best treated with stimulant drugs like methylphenidate (Ritalin), MBD was not based on a clear medical symptom. Quite soon, the modal individual for whom Ritalin became considered the most appropriate treatment was a white and middle-class child. As desegregation was often followed by the new phenomenon of tracking within schools, and as more African American children were labeled as suffering from “mild mental retardation,” the contrasting diagnosis of MBD represented a new disease entity to address the cognitive challenges sometimes faced by privileged children of the predominantly white suburbs. Simultaneously, a growing number of commentators, both African American and anti-racist white, came fiercely to protest what they perceived to be a disturbing tendency to overprescribe stimulant medications to poor children of color.

This concluding chapter discusses the kinds of reforms that are necessary to ensure that all children can receive a free and appropriate public education regardless of their disability status. It first cites data showing that African Americans are still disproportionately tracked in the “mental retardation” and “emotional disturbance” categories while also subject to much higher rates of suspension from school. In contrast, the high-quality private schools for children with autism are more likely to be filled with white children whose parents have been able to take advantage of funding under the Individuals with Disabilities Education Act (IDEA). This chapter also provides suggestions to make the IDEA a more effective tool for children and their families and how it could transform the public schools into a site of excellent education for children with disabilities rather than a mechanism that diverts resources from public schools to private schools.

Iodine is an essential element for human and other animal health and forms an important constituent of the thyroid hormones thyroxine (T4, also known as tetraiodothyronine) and triiodothyronine (T3). These hormones play a fundamental biological role in controlling growth and development (Hetzel and Maberly 1986). If the amount of utilizable iodine reaching the thyroid gland is inadequate, or if thyroid function is impaired, hormone production can be reduced, resulting in a group of conditions collectively referred to as Iodine Deficiency Disorders (IDD) (Fernando et al. 1987, Hetzel 1989). The World Health Organization (WHO 1993) estimate that in excess of one billion people worldwide are at risk from IDD, the most common manifestation of which is goiter (Fig. 9.1). Iodine deficiency is the world’s most common cause of preventable mental retardation and brain damage, and has a significant negative impact on the social and economic development of communities. Although it is likely that IDD are multifactorial diseases involving other trace element deficiencies and goitrogens (goiter-promoting substances) in foodstuffs, a lack of adequate dietary iodine remains a major concern (Stewart and Pharaoh 1996). The link between environmental iodine and IDD has been known for the last 80 years. During this time, the medical community has become well organized when tackling the problem, exemplified by the work of the International Council for the Control of IDD (ICCIDD) ( <https://www.tulane.edu/~icec/icciddhome.htm>), which provides an excellent dissemination point for discussion and information. Remediation strategies often focus on enhancing dietary intakes of iodine via the introduction of iodinated salt and iodinated oil programs (Stanbury and Hetzel 1980). However, these methods are not always successful and other strategies, including environmental interventions, require development (DeLong et al. 1997) In contrast to the wealth of information about the symptoms, assessment, and treatment of IDD, there is very little on the primary cause, a lack of readily available iodine in the environment and diet. Our knowledge of environmental iodine geochemistry is limited, mainly because the analytical methods for assessment are not routine and iodine is not an element that has been systematically determined in geochemical surveys. However, in the past two decades, improved analytical methodologies and an interest in iodine from different perspectives have added much to our knowledge.