al 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.
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 adolescenc