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CLINICAL SYNTHESIS   |    
Overview of Intellectual/Developmental Disabilities
Jarrett Barnhill, M.D., D.F.A.P.A., F.A.A.C.A.P.; Donna McNelis, Ph.D.
FOCUS 2012;10:300-307. doi:10.1176/appi.focus.10.3.300
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Author Information and CME Disclosure

Jarrett Barnhill, M.D., D.F.A.P.A., F.A.A.C.A.P., University of North Carolina School of Medicine, Chapel Hill, NC.

Donna McNelis, Ph.D., Drexel University College of Medicine, Philadelphia, PA.

The authors report no competing interests.

Address correspondence to Jarrett Barnhill, M.D., CB 7160, UNC School of Medicine, Chapel Hill, NC 27599-7160; e-mail: Jarrett_Barnhill@med.unc.edu

Abstract

Patients with intellectual/developmental disabilities (IDD) present many challenges to mental health professionals. The capacity to work with such patients requires a working knowledge of IDD as well as an awareness and understanding of the factors that affect the clinical presentation of mental health disorders across the spectrum of IDD. As with any psychiatric evaluation a thorough history and examination are critical. Input from behavioral specialists, OT, PT, medical/neurological specialists, social workers and psychiatrists is central to the assessment process. But diagnosis can present challenges. The complex nature of both IDD and mental disorders as well as the many faces of diagnostic overshadowing confound differential diagnosis, and many clinicians found it difficult to fit available findings into suitable categories of mental disorders. The publication of the Diagnostic Manual-Intellectual Disability (DM-ID) in 2007 helped alleviate many of these difficulties by providing modified diagnostic criteria that better suit individuals with IDD. Treatment is also multifaceted and most effective when implemented by a team of professionals and not exclusively dependent on psychopharmacological interventions.

Abstract Teaser
Figures in this Article

Intellectual/developmental disabilities (herein referred to as IDD) represent a group of developmental disorders characterized by 1) deficits in measured intelligence and 2) adaptive deficits in self-care, social, self-help, communication, educational, and occupational functioning and 3) an onset prior to age 18 (1, 2). Clinically, this tripartite diagnostic approach casts a wide net and creates a situation in which mental health professionals must deal with a large number of developmental disorders with multiple etiologies. This paper is constructed to assist clinicians in working through some of this complexity and provide some assistance in caring for these patients. Unfortunately we will be unable to discuss all of these issues in great depth but hope to generate sufficient interest to motivate the reader to learn more.

Current lifetime prevalence data suggest that between 20%–70% of individuals with IDD experience significant behavioral problems or meet current diagnostic criteria for a mental disorder (1, 35). These high prevalence rates are linked to the severity of intellectual disability, global impairments in adaptability and resilience, coexisting neurological/medical conditions, histories of major psychosocial and familial dysfunction, and abuse and neglect (57). In addition, life transitions such as physiological changes associated with puberty, the end of educational programs, transitioning to out-of-home living arrangements, declining vigor of aging parents and the physiological effects of aging create major challenges for individuals with IDD. Each of these transitions require major psychological and social adaptation and frequently trigger the onset of both challenging behaviors and the onset of many mental disorders. Unfortunately our clinical understanding of age related changes in brain function, dementias, and other neuropsychiatric conditions are still in their infancy. Much remains to be explored (2, 7).

Each life transition also influences the timing of referrals for mental health services. Most mental health referrals result from increases in troublesome or challenging behaviors (e.g. self-injury or aggression). Because the severity of these behaviors garners immediate attention, the clinician may overlook or not recognize associated primary psychiatric disorders unless a high index of suspicion for their presence is maintained. The reverse can also be true: clinicians can assume that a psychiatric disorder is present even though there is insufficient evidence to make an appropriate diagnosis. For example hallucinations prompt the diagnosis of schizophrenia regardless of contradictory findings or other core features of this severe mental illness.

Why might such misdiagnoses occur? Many patients with IDD are frequently unable to adequately describe mood or cognitive states because of limited expressive language, difficulty describing such internal states, or are subject to regression and cognitive/behavioral disorganization in response to environmental stressors. In addition, some are unable to provide useful information or fully understand the process of the psychiatric examination. As a result the clinician must rely on secondary sources or direct observation, inference and extrapolation of complex behaviors to fit the diagnostic criteria of psychiatric disorders. In addition, a failure to consider the contribution of medical or neurological illness or medication side effects on challenging behaviors can lead to misdiagnosis of serious organic mental disorders (e.g. delirium) as primary mental illness. Such misdiagnoses can also lead to further complications secondary to inappropriate treatment strategies.

To accommodate these complex features of neurodevelopmental disorders we will expand the usual definition of diagnostic overshadowing (misattributing symptoms of mental illness to IDD) to include behavioral changes associated with neurological and medical disorders. Thus the misdiagnosis of medical/neurological disorders as primary psychiatric conditions and misdiagnosis of primary psychiatric conditions as medical/neurological disorders are added diagnostic overshadowing. Resolving these issues requires a high index of suspicion and a reasonable working knowledge of neuropsychiatry. Such awareness can improve our understanding of the complex nature of differential diagnosis and help us empathize with the problems faced by colleagues working in the field of dual diagnosis (IDD and MH) (2).

A second set of challenges may be as complicated as those outlined above. Understanding and treating individuals with dual diagnosis also forces the clinician to integrate multiple clinical perspectives. For example:

  • Behavioral therapy and learning theory: This system is based on target behaviors rather than syndromes (e.g. aggression in response to changes in key environmental factors or escape from task demands) (8). The challenge to mental health professionals is to determine when appropriate target symptoms are identified with specific psychiatric syndromes, e.g. dysphoric mood in major depressive disorder.

  • Nomenclature issues: Clinicians need to adapt our current nomenclature to better fit adult patients with IDD. The Diagnostic Manual-Intellectual Disability (DM-ID) and the Diagnostic Criteria-Learning Disorders respectively represent attempts to adapt the DSM-IV-TR and ICD-9 uniquely to these differences in nosology.

  • Adapting to multidisciplinary teams. Best practices in the field of dual diagnosis include mental health professionals as part of a team that includes behavioral psychologists, occupational therapists, physical therapists, pediatric neurology, medicine, psychiatry, educators, family members, and direct support professionals and others. The goal is to integrate different points of view and treatment models into a coherent treatment plan (57).

A third challenge arises from an information explosion in the clinical neurosciences of IDD and mental illness. At a practical level we need to translate new information into clinical practice. At a theoretical level we need to update the biopsychosocial model to include:

  • Genetics: Genes serve as the blueprint for brain development. Our older models were deterministic, hence a nature-nurture debate; current models are probabilistic and interactional. Clinical researchers moved beyond Mendelian (autosomal dominant, recessive inheritance) analysis and now emphasize the sequence and integration of gene activation and de-activation during critical periods of development. As a result the focus instead is on epigenetics and gene-environmental interactions. In this world, the nature-nurture argument is an anachronism (911).

  • Neurosciences: Rapid advances in the neurosciences are deepening our understanding of central coherence, executive functions and adaptive behaviors, theory of mind, social communication, memory, attention, impulse control and affect regulation (11). Our challenge is to understand how errors in brain development (errors in neuronal migration, maturation, neuroplasticity, myelinization and interactive specialization and regional interconnections) relate to cognitive, social and emotional development; and how these errors translate into real life problems for adults with dual diagnoses.

  • Translational research needs: Clinicians concentrate on challenging behaviors and mental disorders and often eschew molecules as well as policy. But we cannot lose sight of the interactions between macrocosmic forces such as socio-cultural, governmental and economic forces and microcosmic ones related to genetics and neurobiology.

As a result, we need to redefine our understanding of the biopsychosocial model to incorporate this new knowledge (12). The challenge for the 21st century is to adapt the biopsychosocial model in order to make sure that our ideas about the multidirectional and systemic forces underlying this concept are kept up to date with scientific and clinical reality. Translating the innovations in the neurosciences into best practices, positive practice models, and evidence-based and outcome-based treatment for busy clinicians is one of our greatest challenges.

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Deficits in measured intellectual/cognitive abilities are not enough

IDD are most often considered in terms of performance on individualized measures of intelligence. Historically, the development and introduction of intelligence testing represented a major breakthrough in our ability to measure and classify IDD. But it wasn’t long before researchers and clinicians realized that normalized measures of intelligence provided only a portion of what was needed. Yet in many programs, service providers still use IQ scores to group patients into broad categories (mild, moderate, severe, and profound levels of ID). As we shall see, this view is incomplete (6, 13)

In educational settings, this IQ score shorthand is used in decision-making about classroom placement, setting performance expectations as well as designing educational programs to match academic and daily life skills training needs. Yet the validity of these predictions is often derailed by positive effects of early intervention and better management of neurodevelopmental disorders such as seizures and the negative effects of severe behavioral problems, neuropsychiatric and medical disorders (e.g., cerebral palsy or epilepsy). In addition, disruptive behaviors and the presence of unrecognized or inadequately treated mental disorders have a deleterious effect on educational performance (14). These persist into adulthood as behavioral problems that adversely affect structured employment, community independence, social activities, and residential living and produce levels of psychosocial stress on caregivers and alter the quality of life (7).

Psychodynamic-oriented clinicians use IQ scores to formulate hypotheses about their role in psychosexual, psychosocial and cognitive development. The relationship between mental age and developmental stages is a permeable one but these data do provide a system of staging strengths and vulnerabilities and clarify developmental levels of functioning. Within a psychodynamic framework, arrests and derailments of many lines of development underlie working hypotheses about the sources of challenging behaviors and how these may represent manifestations of various mental disorders. This system is less often applied and often less useful in the presence of severe IDD, cerebral palsy, epilepsy and other neurological, genetic disorders (including recognizable behavioral phenotypes) (7, 15).

In the final analysis, it is a combination of these models with behavioral and neuropsychological data that help us integrate biology, past life experiences and psychological development into our understanding of aggression, self-injurious behavior (SIB), hyperactivity and stereotypies. The increased use of attachment and separation-individuation models are providing additional insights into how an individual with IDD adapts and responds to his psychosocial environment (16). In addition, ethology, neuro-ethology and behavioral pharmacology are becoming useful tools in understanding complex social behaviors such as aggression or avoidance behaviors. This information may be as valuable as measured intellectual abilities in explaining what initiates and maintains these behaviors.

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Deficits in adaptive skills are more than meets the eye

Adaptive skills represent an amalgam of abilities associated with 1) behavioral flexibility, 2) experiential learning (“plastic” intelligence), 3) problem solving, 4) coping with novel settings 5) task demands (procedural learning) and 6) mastery of skills of daily living. Social intelligence is another subset of adaptive skills that do not seem directly tied to other forms of intelligence but play a key role in all forms of skill learning (14). This relative disconnect reinforces the importance of adaptive skills in the definition of IDD.

For example, individuals with mild IDD may have sufficient adaptive skills to “disappear” into the workday world after completing school. In general, their cognitive limitations are camouflaged by good communication and reasonable adaptive skills. Yet abuse/neglect, coexisting developmental disorders (e.g., autism spectrum disorder or cerebral palsy) and mental disorders can derail this more favorable developmental trajectory (15). From a neuropsychological perspective, early environmental insults can adversely affect behavior regulation, cognitive flexibility, stress management as well as lower the threshold for major mental disorders. For many supportive caregivers, positive learning experiences and the availability and utilization of individually-directed and designed programs can compensate for these psychosocial insults and improve outcome by enhancing resilience and coping skills.

Individuals with severe-profound IDD (SPIDD) present a different picture. These individuals may lack the intellectual or adaptive capacities to deal with many routine life experiences. The increased prevalence of genetic, neurological, medical and other developmental disorders limit the pace of learning and can produce less reversible ceiling effects on adaptive skills (15, 17). Yet individuals with SPIDD are more likely to respond to physiological and psychological distress by increases in the frequency or severity of either pre-existing or new patterns of challenging behaviors (baseline exaggeration). For example, changes in expected routine or caregiver can be highly stressful events. Because of limited communication skills, challenging behaviors become the primary mode of expressing distress or pain. Understanding and interpreting these behavioral responses can require a combination of provider familiarity and clinical savvy.

Problems arise when clinicians misattribute these transient or environmentally driven changes in behavior (baseline exaggerations, behavioral regression and cognitive disorganization) as a primary neuropsychiatric disorder. The reverse can also be true: the emergence of a primary psychiatric disorder may increase the individual’s vulnerability to that stress or be the cause of the reaction. Impaired adaptive skills can become a setting event, contributing factor, or an impediment to the natural resolution or the underlying factor in the diagnostic misattribution.

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Onset during the developmental period

The developmental period is most often defined as between birth and age 18. Although useful for legal and guardianship purposes, this legalistic cutoff is inconsistent with current models of neurodevelopment. Research suggests that brain maturation and neuroplasticity continue well past age 18. For individuals with IDD, ongoing brain development suggests a lifelong capacity for skill learning, provided the individual is free of neurodegenerative, neuropsychiatric or medical illnesses. But there is a paradox inherent to this observation. The timing of any insult on brain development is complex and incompletely understood. There are fundamental neurobiological differences between acquired lesions in adulthood and those occurring during critical periods in brain development. Even though some insults during infancy are more amenable to interventions, there may still be potential limits imposed on later developing neurocognitive skills. The critical piece is the timing of the intervention: early and intensive intervention during periods of rapid brain development is most effective for many but not all areas of development.

Many genetic syndromes present another twist: the age of onset is often inversely related to the severity, clinical course and prognosis. Milder forms of autosomal disorders present with minimal findings during childhood but then emerge and slowly progress during adolescence or early adulthood. Classification based on a cutoff age of 18 becomes confusing when there is a very slow cognitive decline (drop in IQ score and decreasing adaptive skills) that is finally recognized in late adolescence. This scenario is more consistent with neurodegenerative or dementing illness that was masked by learning disability or low normal intelligence until clear cut neurological or metabolic symptoms emerged. Both traumatic brain injury and the onset of neurodegenerative disorders during late adolescence may contribute to behavioral or mental health problems prior to obvious cognitive decline. This gap can make it more difficult to determine the age of onset issue.

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Genes and developmental disabilities

The number of genetic syndromes is growing in conjunction with the development of new genetic techniques. 30 years ago genetic testing usually meant chromosome testing and linkage studies. Nowadays we can obtain genome wide scans, florescence in situ hybridization, and microarrays that hone in on single nucleotide polymorphisms, copy number variants and the structure of specific genes (18). Recent breakthroughs in Fragile X research have opened another doorway with the discovery that mglut5 antagonists appear to reverse both molecular and cognitive/behavioral features of Fragile X (18, 19). There is growing research in epigenetics that point to changes in genes regulation due to trauma or faulty parenting. These findings challenge genetic determinism and force us to rethink nature-nurture arguments in terms of a newer understanding of gene–environment interactions.

Behavioral phenotypes are patterns of cognition and behavior associated with specific genetic disorders. Examples include: gaze aversion and anxiety in Fragile X (20); hyperphagia and binge eating in Prader Willi syndrome (21); personality traits linked to Trisomy 21 (22); increased risk for schizophrenia in 22q deletion (Velocardiofacial syndrome) (23); and epilepsy, dysmorphologies, hypotonia, and autism in 15q11.2-13 duplications (24). Many behavioral phenotypes bear some resemblance to temperamental features of affected individuals. Others seem more like prodromal primary psychiatric disorders (18). Unfortunately, there are too many genetic and neuroanatomical “smoking guns” for polygenic disorders like psychosis, bipolar disorder/schizophrenia, autism, and epilepsy in patients with IDD. This observation suggests that we are dealing with complex disorders and reinforces the idea that many syndromes are related to disruptions in pathways rather than specific lesions or related to single neurotransmitter abnormalities.

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Sociocultural influences

The most commonly neglected component of the biopsychosocial model is the role played by socio-cultural forces in dual diagnosis. Over the past three centuries, attitudes and values about individuals with IDD changed dramatically. These changes impact the social risk factors on the epidemiology, availability and types of habilitation and treatment services for those with IDD and mental disorders. In industrialized societies, urbanization and changing modes of living and working placed new occupational and educational demands that changed the niche occupied by individuals with ID. For example, many individuals with IDD now live in a society where there are fewer less technologically demanding jobs (requiring basic skill sets) and these jobs are often subject to increasing competition. These social changes are complicated by smaller families, greater geographic mobility and the problem of isolation from traditional sources of family support. Today families rely upon “professional services” to fill this void (8).

These social and cultural changes are redefining our sense of community. Historically, attitudes such as relative pessimism by medical providers about a lack of effective interventions and prognosis; marginalization and socio-economic segregation of individuals and their families; and lack of community-based resources contributed to out-of-home residential placement. Governmental actions focused mainly on developing programs that eventually became large custodial institutions (25). As an outgrowth of the Civil and Human Rights movement and numerous lawsuits, there is a shift to community care, inclusion, freedom of choice, active treatment and protection from various forms of restraint. But these changes are quite vulnerable to economic downturns; legislative battles ensue over cost-effectiveness instead of treatment efficacy. Unfortunately, there has been a resurgence of ambivalence about placing group homes in residential neighborhoods as well as availability and adequate resources for staff and educators. Finally, limitations on funding and access to an integrated system of comprehensive health and mental health care (26) are present in many states. The care of high service users such as those with dual diagnosis is especially vulnerable to these socio-political forces (8, 2729). This unfortunate scenario may underlie the recent trends toward increasing use of psychotropic drugs (30, 31).

It is also important to recognize a selection bias inherent in most mental health referrals. Since referrals arise due to disruptive, destructive, self-injurious behaviors or irritable/aggressive behaviors we must maintain a high index of suspicion for unrecognized psychiatric or medical/neurological disorders. Sorting out these generic referrals is the function of differential diagnosis. The following steps are useful in this process:

  • Data collection and decision making: Collect medical, psychiatric and developmental histories—both indirect reports and direct observations—and data from available rating scales. Convert this information into a timeline to create a visual representation of behavioral or symptom change through time. Converting behavioral information into a graphic format permits the clinician to track both behavioral data but also to integrate syndrome change (e.g. bipolar disorder); severity and intensity measures; and findings from serial mental status and rating scales. The Assessment of Dual Diagnosis (ADD) (32), the Emotional Problems Scale: Behavior Ratings Scale (EPS-R) (33) and The Diagnostic Assessment for the Severely Handicapped-II (34) are informant–based rating scales that cross-walk with the DSM-IV TR. The ADD and EPS-R were developed for patients with mild to moderate IDD whereas the DASH-II was developed for patients with SPIDD. Treatment response can also fit into this scheme (15).

  • Management of medical/neurological and laboratory data: Include and integrate relevant baseline medical studies, available information on genetic and metabolic disorders, neurophysiological and neuroimaging studies. These data need to be formulated for each phase of this outline for differential diagnosis. Clinical screening and neuropsychological testing are useful when dementia is suspected (35, 36).

  • Integrate medical/psychiatric assessment with functional behavioral analysis: Missing from many functional behavioral analyses are information about temperament, level of emotional reactivity, neuroticism, patterns of attachment, preponderance of approach/avoidance behaviors, emotional regulation, and level of impulse control. These neurobiological traits can profoundly influence a patient’s vulnerability to specific antecedents or triggers (8). For example, individuals with a history of severe abuse may be hypersensitive to being left alone at night, or attempts to set limits (18, 37, 38). This data may help explain what appears to be a persistent, disproportionate and treatment resistant reaction. A similar expanded mode of analysis involves both motivational and sustaining factors. For example, state-related anhedonia in major depression can reduce the reinforcement efficacy of social contact or favored activity (39). Likewise negative emotional reactions to novel situations or new staff or fear noted above should determine the pace of changes in behavioral programming (35, 37, 40, 41).

  • Social context of behaviors: Aggression (42), self-injury and other target behaviors occur in a social context. For many patients with SPIDD, aggression or SIB can represent forms of social communication (43) or expressions of attachment, dominance and territorial disputes (e.g. whose chair is this?). Psychiatric disorders also occur within and affect social networks, families, school and in work settings. Formulating this data may be more useful than a simple Axis V number in treatment planning (8, 44).

  • The last step is developing a multiaxial, psychiatric diagnosis. In the past there was difficulty matching the patient to the diagnostic criteria that were not adapted to the special issues associated with IDD. Fortunately the Diagnostic Manual-Intellectual Disability and Diagnostic Criteria-Learning Disability are now available to assist clinicians in negotiating a clinical diagnosis.

The diagnosis and treatment of mental disorders in adults with IDD requires that the clinician is able to negotiate two worlds. As a team member, the psychiatrist often plays the role of translator between the world of the neurosciences and biomedicine and the team. As we have seen, the differential diagnosis can present some of our greatest challenges. For example, schizophrenia is frequently diagnosed and treated based on the presence of hallucinations or delusions without a comprehensive exploration of psychosis; psychotic forms of major depressive, bipolar disorder, PTSD, delirium, dissociative states and intoxication can occur (3). A parallel problem arises when clinicians prescribe psychopharmacological treatment for aggression, self-injury, agitation and disruptive/destructive behaviors without thorough reviews of environmental factors (social ecology), review of neurobiological setting events and functional behavioral analyses. In either of these scenarios the rush to treat can result in the long-term exposure but often ineffective treatment regimens that all too often result in unnecessary polypharmacy (30, 44).

Traditionally, most mental health clinicians accept the view that mental disorders arise from the interaction between psychosocial stresses and biological/genetic risks for a particular mental disorder (“two hit theories”). Some colleagues take a different approach, viewing challenging behaviors as learned phenomena. These behavioral specialists tend to focus less on accurate diagnosis and biogenetic etiology (8). Yet in light of our current knowledge, neither approach provides the ultimate solution. As clinicians we need to consider both challenging behaviors and mental disorders as lying on a continuum. From this perspective, challenging behaviors are attributed to environmental stressors and patterns of reinforcement or consequences; mental disorders, consequences of complex gene-environmental interactions. On closer analysis, gene-environmental interactions also bias the individual toward specific behavioral reactions to specific circumstances and the risk for psychiatric disorders. Sorting out these complex relationships and matching them with current evidence-based treatment or best practices are some of our greatest challenges.

Mental health professionals entering the world of IDD and dual diagnosis must be open to learning from other disciplines while thinking through problems both systemically and systematically. The time-consuming, multidisciplinary nature of assessment, diagnosis and treatment planning requires understanding of many bodies of knowledge. For psychiatrists, the challenge is to view psychopharmacological interventions as but one component of a complex toolkit (Table 1).

 
Anchor for Jump
Table 1.Psychopharmacology Pearls for Patients with IDD

The field of IDD and dual diagnosis requires that the clinician maintain a good working knowledge of ongoing research in the behavioral and developmental neurosciences and psychopharmacology. As more data become available on behavioral phenotypes, epigenetics, and behavioral pharmacology, the clinician will be required to synthesize this new data with existing behavioral and mental health practices. The old approaches relying upon behavior/psychiatric disorder, nature/environment versus nurture/genetic risk, organic/functional disorders will need to be revised. These changes will bring us to conclude:

  • Brain behavioral relationships are too complex to be conceptualized in terms of single anatomical sites or neurotransmitters. Treating based on suspected neurotransmitter abnormalities are woefully reductionist and may lead to unnecessary polypharmacy.

  • Challenging behaviors and psychiatric disorders are heterogeneous phenomena that cannot be fully captured by a traditional behavioral analysis or psychiatric diagnosis. We will need to adapt our thinking to ongoing work on subtyping challenging behaviors and endophenotypes of primary psychiatric disorders. We will need to sharpen our diagnostic skills to meet this challenge and adapt our treatment planning to match this new knowledge.

  • Alternative treatments such as transcranial magnetic stimulation, deep brain stimulation and models of neuropharmacology that focus on intracellular mechanisms and alterations in gene regulation are on the horizon. This shift will require us to understand the basic neurobiology of developmental disorders; how it differs from neuro-typical patients, and what special adjustments we will need to make to accommodate these differences (35, 45).

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[CrossRef]
 
Barnhill  LJ:  Can the DSM-IV-TR Be Saved for Individuals with Intellectual Disability? Ment Health Aspects Dev Disabil 2003; 6:85–99
 
Urv  TK;  Zigman  WB;  Silverman  W:  Psychiatric symptoms in adults with Down syndrome and Alzheimer’s disease.  Am J Intellect Dev Disabil 2010; 115:265–276
[PubMed]
[CrossRef]
 
Murphy  GH;  O’Callaghan  AC;  Clare  ICH:  The impact of alleged abuse on behaviour in adults with severe intellectual disabilities.  J Intellect Disabil Res 2007; 51:741–749
[PubMed]
[CrossRef]
 
Nanni  V;  Uher  R;  Danese  A:  Childhood maltreatment predicts unfavorable course of illness and treatment outcome in depression: a meta-analysis.  Am J Psychiatry 2012; 169:141–151
[PubMed]
[CrossRef]
 
Sohanpal  SK;  Deb  S;  Thomas  C;  Soni  R;  Lenôtre  L;  Unwin  G:  The effectiveness of antidepressant medication in the management of behaviour problems in adults with intellectual disabilities: a systematic review.  J Intellect Disabil Res 2007; 51:750–765
[PubMed]
[CrossRef]
 
Charlot  L;  Deutsch  CK;  Albert  A;  Hunt  A;  Connor  DF;  McIlwane  WJ:  Mood and Anxiety disorders in Psychiatric Inpatients with Autism Spectrum Disorders and Depression.  J Mental Health Research in Intellectual Disabilities 2008; 1:238–254
[CrossRef]
 
Wigham  S;  Hatton  C;  Taylor  JL:  The Effects Traumatizing Life Events on People with Intellectual Disabilities: A Systematic Review.  J Mental Health Research in Intellectual Disabilities 2011; 4:19–40
[CrossRef]
 
Crocker  AG;  Mercier  C;  Allaire  J-F;  Roy  M-E:  Profiles and correlates of aggressive behaviour among adults with intellectual disabilities.  J Intellect Disabil Res 2007; 51:786–801
[PubMed]
[CrossRef]
 
Petty  J;  Allen  D;  Oliver  C:  Relationship among challenging, repetitive, and communicative behaviors in children with severe intellectual disabilities.  Am J Intellect Dev Disabil 2009; 114:356–368
[PubMed]
[CrossRef]
 
Davis  E;  Barnhill  LJ;  Saeed  SA:  Treatment models for treating patients with combined mental illness and developmental disability.  Psychiatr Q 2008; 79:205–223
[PubMed]
[CrossRef]
 
Barnhill  LJ:  The diagnosis and treatment of individuals with mental illness and developmental disabilities: an overview.  Psychiatr Q 2008; 79:157–170
[PubMed]
[CrossRef]
 
References Container
Anchor for Jump
Table 1.Psychopharmacology Pearls for Patients with IDD
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References

American Psychiatric Association: Diagnostic and Statistical Manual, 4th Ed. Text Revision. Washington, DC, 2000.
 
Fletcher  R;  Loschen  E;  Stavrakaki  C;  First  M (ed):  Diagnostic Manual-Intellectual Disability (DM-ID): A Textbook of Diagnosis of Mental Disorders in Persons with Intellectual Disability .  Kingston, NY,  The NADD Press, 2007
 
Kitamura  H;  Shioiri  T;  Itoh  M;  Sato  Y;  Shichiri  K;  Someya  T:  Does operational diagnosis of schizophrenia significantly impact intellectual deficits in psychotic disorders? J Intellect Disabil Res 2007; 51:812–820
[PubMed]
[CrossRef]
 
Hove  O;  Havik  O:  Mental Disorders and Problem Behaviors in a Community Sample of Adults with Intellectual Disability: Three Months Prevalence and Comorbidity.  J Mental Health Research in Intellectual Disabilities. 2008; 1:223–238
[CrossRef]
 
Myrbakk  E;  von Tetzchner  S:  The Prevalence of Behavioral Problems among People with Intellectual Disability Living in Community Settings.  J Mental Health Research in Intellectual Disabilities 2008; 1:205–222
[CrossRef]
 
Melanoscino  F;  Stark  J (ed):  Handbook of Mental Illness in the Mentally Retarded .  New York,  Plenum Press, 1984
 
Harris J: Intellectual Disability, New York: Oxford University Press; 2006.
 
Barnhill  J:  The Differential Diagnosis of Childhood Developmental Disorders.  Psychiatric Times 2008; 25:36–41
 
Ridley  M:  Nature via Nurture: Genes, Experience and What Makes Us Human. ISBN-0-06-000678-1 New York   Harper Collins Publishers, 2002, pp 125–200
 
El-Fishaway  P;  Stite  MW:  Genetics of Autism: Key Issues, Recent Findings and Clinical Implications.  Psychiatr Clin North Am 2011; 33:81–105
 
Rutter  M:  The interplay of nature, nurture, and developmental influences: the challenge ahead for mental health.  Arch Gen Psychiatry 2002; 59:996–1000
[PubMed]
[CrossRef]
 
Ghaemi  N:  The Rise and Fall of the Biopsychosocial Model: Reconciling Art and Science in Psychiatry. Baltimore ISBN: 13   Johns Hopkins Press, 2010., 252 pp
 
Bourus  N (ed):  Mental Health in Mental Retardation .  New York,  Cambridge Univ Press, 1994
 
Barnhill  LJ;  de Koning  ND;  Poindexter  AR:  Other disorders of infancy, childhood or adolescence, in  Diagnostic Manual-Intellectual Disability: A Textbook of Diagnosis of Mental Disorders in Persons with Intellectual Disability (DM-ID) . Edited by Fletcher  R;  Loschen  E;  Stavrakaki  C;  First  M.  Kingston, NY,  NADD Press, 2007
 
Woolf  S;  Woolf  CM;  Oakland  T:  Adaptive behavior among adults with intellectual disabilities and its relationship to community independence.  Intellect Dev Disabil 2010; 48:209–215
[PubMed]
[CrossRef]
 
Matson  J;  Laud  R;  Matson  M (ed):  Behavior Modification in Persons with Developmental Disabilities . vol. 1.  Kingston, NY,  NADD Press, 2004
 
Turk  J;  Robbins  I;  Woodhead  M:  Post-traumatic stress disorder in young people with intellectual disability.  J Intellect Disabil Res 2005; 49:872–875
[PubMed]
[CrossRef]
 
Finucane  B;  Haas-Givler  B:  Smith-Magenis Syndrome: Genetic Basis and Clinical Implications.  J Mental Health Research in Intellectual Disabilities 2009; 2:134–148
[CrossRef]
 
Smith  LE;  Barker  ET;  Seltzer  MM;  Abbeduto  L;  Greenberg  JS:  Behavioral phenotype of fragile X syndrome in adolescence and adulthood.  Am J Intellect Dev Disabil 2012; 117:1–17
[PubMed]
[CrossRef]
 
Levitas  A;  Dykens  E;  Finucane  B;  Kates  W:  Behavioral phenotypes of genetic disorders, in  Diagnostic Manual-Intellectual Disability . Edited by Fletcher  R;  Loeschen  E;  Stavrakaki  C;  First  M.  Kingston,  NADD Press, 2007
 
Woodcock  KA;  Oliver  C;  Humphreys  GW:  A specific pathway can be identified between genetic characteristics and behaviour profiles in Prader-Willi syndrome via cognitive, environmental and physiological mechanisms.  J Intellect Disabil Res 2009; 53:493–500
[PubMed]
[CrossRef]
 
Hepburn  SL;  McLean  WE:  Maladaptive and Repetitive Behaviors in Children with Down Syndrome and Autistic Spectrum Disorders: Implications for Screening.  J. Mental Health Research in Intell Disabilities 2009; 2:65–162
[CrossRef]
 
Gothelf  D;  Frisch  A;  Michaelpvsky  E;  Weizman  A;  Sprintzen  RJ:  Velocardiofacial Syndrome.  J. Mental Health Research in Intell Disabilities 2009; 2:149–162
[CrossRef]
 
Eapen  V:  Genetic basis of autism: is there a way forward? Curr Opin Psychiatry 2011; 24:226–236
[PubMed]
[CrossRef]
 
Wolfensberger  W:  Will there always be an institution? II: the impact of new service models—residential alternatives to institutions.  Intellect Dev Disabil 2011; 49:425–434
[PubMed]
[CrossRef]
 
Chowdhury  M;  Benson  B:  De-institutionalization and Quality of Life of Individuals with Intellectual Disability: A Review of the International Literature.  J Policy Pract Intell Disabil 2011; 8:256–259
[CrossRef]
 
Kozma  A;  Mansell  J;  Beadle-Brown  J:  Outcomes in different residential settings for people with intellectual disability: a systematic review.  Am J Intellect Dev Disabil 2009; 114:193–222
[PubMed]
[CrossRef]
 
Hartley  SL;  Maclean  WE:  Depression in adults with mild intellectual disability: role of stress, attributions, and coping.  Am J Intellect Dev Disabil 2009; 114:147–160
[PubMed]
[CrossRef]
 
Emerson  E;  McCulloch  A;  Graham  H  et al:  Socio-economic Circumstances and Risk of Common Psychiatric Disorders among Parents of Young Children with and Without Early Cognitive Delay.  Am J Intell Develop Disabilities 2010; 115:30–42
[CrossRef]
 
Deb  S;  Sohanpal  SK;  Soni  R;  Lenôtre  L;  Unwin  G:  The effectiveness of antipsychotic medication in the management of behaviour problems in adults with intellectual disabilities.  J Intellect Disabil Res 2007; 51:766–777
[PubMed]
[CrossRef]
 
Courtemanche  AB;  Schroeder  SR;  Sheldon  JB:  Designs and analyses of psychotropic and behavioral interventions for the treatment of problem behavior among people with intellectual and developmental disabilities.  Am J Intellect Dev Disabil 2011; 116:315–328
[PubMed]
[CrossRef]
 
Matson  JL;  Bamburg  JW:  Reliability of the assessment of dual diagnosis (ADD).  Res Dev Disabil 1998; 19:89–95
[PubMed]
[CrossRef]
 
Strohmer  D;  Prout  H:  Emotional Problem Scales: Behavior Rating Scales .  Schenectady, NY,  Genium Publishing, 1991
 
Matson  JL;  Gardner  WI;  Coe  DA;  Sovner  R:  A scale for evaluating emotional disorders in severely and profoundly mentally retarded persons. Development of the Diagnostic Assessment for the Severely Handicapped (DASH) scale.  Br J Psychiatry 1991; 159:404–409
[PubMed]
[CrossRef]
 
Barnhill  LJ:  Can the DSM-IV-TR Be Saved for Individuals with Intellectual Disability? Ment Health Aspects Dev Disabil 2003; 6:85–99
 
Urv  TK;  Zigman  WB;  Silverman  W:  Psychiatric symptoms in adults with Down syndrome and Alzheimer’s disease.  Am J Intellect Dev Disabil 2010; 115:265–276
[PubMed]
[CrossRef]
 
Murphy  GH;  O’Callaghan  AC;  Clare  ICH:  The impact of alleged abuse on behaviour in adults with severe intellectual disabilities.  J Intellect Disabil Res 2007; 51:741–749
[PubMed]
[CrossRef]
 
Nanni  V;  Uher  R;  Danese  A:  Childhood maltreatment predicts unfavorable course of illness and treatment outcome in depression: a meta-analysis.  Am J Psychiatry 2012; 169:141–151
[PubMed]
[CrossRef]
 
Sohanpal  SK;  Deb  S;  Thomas  C;  Soni  R;  Lenôtre  L;  Unwin  G:  The effectiveness of antidepressant medication in the management of behaviour problems in adults with intellectual disabilities: a systematic review.  J Intellect Disabil Res 2007; 51:750–765
[PubMed]
[CrossRef]
 
Charlot  L;  Deutsch  CK;  Albert  A;  Hunt  A;  Connor  DF;  McIlwane  WJ:  Mood and Anxiety disorders in Psychiatric Inpatients with Autism Spectrum Disorders and Depression.  J Mental Health Research in Intellectual Disabilities 2008; 1:238–254
[CrossRef]
 
Wigham  S;  Hatton  C;  Taylor  JL:  The Effects Traumatizing Life Events on People with Intellectual Disabilities: A Systematic Review.  J Mental Health Research in Intellectual Disabilities 2011; 4:19–40
[CrossRef]
 
Crocker  AG;  Mercier  C;  Allaire  J-F;  Roy  M-E:  Profiles and correlates of aggressive behaviour among adults with intellectual disabilities.  J Intellect Disabil Res 2007; 51:786–801
[PubMed]
[CrossRef]
 
Petty  J;  Allen  D;  Oliver  C:  Relationship among challenging, repetitive, and communicative behaviors in children with severe intellectual disabilities.  Am J Intellect Dev Disabil 2009; 114:356–368
[PubMed]
[CrossRef]
 
Davis  E;  Barnhill  LJ;  Saeed  SA:  Treatment models for treating patients with combined mental illness and developmental disability.  Psychiatr Q 2008; 79:205–223
[PubMed]
[CrossRef]
 
Barnhill  LJ:  The diagnosis and treatment of individuals with mental illness and developmental disabilities: an overview.  Psychiatr Q 2008; 79:157–170
[PubMed]
[CrossRef]
 
References Container
+
+

CME Activity

Add a subscription to complete this activity and earn CME credit.
Sample questions:
1.
Over the past few decades, a major factor increasing the burden on families of chronically ill children has been:

See Smith and Kaye, Introduction, p 255
2.
An often unrecognized psychological dynamic with the parents of chronically ill children is guilt over:

See Smith and Kaye: The Psychological Experience of Parents and Caregivers, p 256
3.
Diagnostic overshadowing is a frequent problem for mental health professionals assessing individuals with severe IDD. Which of the following best describes this problem?

See Barnhill and McNelis: Epidemiology and Natural History, p 300
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