On June 16, 2009, Qsac held its annual workshop for parents and professionals at the Sheraton La Guardia Hotel. A group of experts on autism discussed the complexity of social behavior in autism, screening, diagnosis and treatment strategies, applied behavior analysis and discrete trial training. During a panel, one of the participants asked a question about the prognosis of autism. This is a very challenging question because of the heterogeneity within the autism diagnosis, which affect our ability to develop an effective treatment and prognosis. Autism is a neurodevelopmental disorder that has been defined exclusively on behaviorally based symptom domains of impairments in social interactions and communication, and repetitive or stereotypical behaviors (DSM-IV-TR,
From a clinical point of view, the diagnosis have shown a range of variability in the core symptom domains, including a low to above normal IQ, and low to high functioning in school (Bailey et al., 1998; Spence, 2001; Silverman et al., 2002; Folstein et al., 1998; Spiker, 1999; Beglinger and Smith, 2001; Spiker et al., 2002)
In terms of the research studies, we can observe a lack of consistency and uniformity. Although autism disorder is under the “pervasive developmental disorder” (
According to Miles and colleagues (2005), some genetic studies have focused on the correlation of genetic indicators with behavioral symptoms, cognition, and core symptom domains such as language impairment.
Miles and colleague (2003, 2005), defined autism spectrum disorder from a genetic etiological point of view into two subgroups, (1) Idiopathic, in which no cause can be identified and represents 90-95% of the cases with autism; and (2) Secondary, in which chromosome abnormality, single-gene disorder or environmental agents can be identified and represents 5-10%.
Idiopathic autism can be divided in (a) complex autism and (b) essential autism. The complex autism is characterized by the presence of a significant number of physical anomalies, lower male to female ratio and / or microcephaly in 5-15% of cases; they scored with lower IQ, experience more seizure and /or abnormal EEG’s and more abnormal findings, and represent 20-30% of the autistic population. The essential autism is characterized by no evidence of abnormal structure during development [morphogenesis] and represents70% of the autistic population.
The essential and complex groups are relatively easy to identify clinically, and appear to differ in their outcomes, recurrence risks, sex ratios, and family histories (Miles et al., 2000, 2003, 2005.) For instance, the ratio of males vs. females in essential autism is greater than in individuals with complex autism (6.5:1). This classification of autism between complex and essential autism helps to clarify the etiologic heterogeneity within the autism spectrum disorders. However, until we separate the genetic indicators of the behavioral autism, it would be very difficult to understand the prognosis of autism spectrum disorder.
The prognosis will vary depending of the phenotype features of the autistic disorder [e.g. the observable physical or biochemical characteristics of an individual, as determined by both genetic makeup and environmental influences.] For instance, the prognosis of an autistic individual with idiopathic autism may be better than an individual with secondary autism; an individual with idiopathic autism-complex may have a worse prognosis than an individual with idiopathic essential-autism. This classification between idiopathic and secondary opens a debate about the heterogeneity and clinical variability of autism, which has prompted some researchers to use the term Autisms instead of autism (Pardo & Eberhart, 2007; Miles & Hillman, 2003; Herbert, 2003, 2005.)
To talk about the prognosis of autism becomes more complex since some research evidences have pointing out the genetics alone do not determine the entire Autism Spectrum Disorder, it is only a risk, and non-genetic factors are playing an important role as modifiers of processes determined by genetic susceptibility (e.g. environmental and epigenetic factors) (Pardo & Eberhart, 2007; Hebert, 2004, 2005.)
The prognosis of autism(s) would be better understood when researchers are able to determine the different variations in autism(s) and their genetic-environmental-timing influences.