There are few studies of long-term effects, and there is a lack of clarity about the presentation of the disorder beyond the age of five years. However, the opening of orphanages in Eastern Europe following the end of the Cold War in the early 1990s provided opportunities for research on infants and toddlers brought up in very deprived conditions. Such research broadened the understanding of the prevalence, causes, mechanism and assessment of disorders of attachment and led to efforts from the late 1990s onwards to develop treatment and prevention programs and better methods of assessment. Mainstream theorists in the field have proposed that a broader range of conditions arising from problems with attachment should be defined beyond current classifications.Mainstream treatment and prevention programs that target RAD and other problematic early attachment behaviors are based on attachment theory and concentrate on increasing the responsiveness and sensitivity of the caregiver, or if that is not possible, placing the child with a different caregiver. Most such strategies are in the process of being evaluated. Mainstream practitioners and theorists have presented significant criticism of the diagnosis and treatment of alleged reactive attachment disorder or the theoretically baseless "attachment disorder" within the controversial form of psychotherapy commonly known as attachment therapy. Attachment therapy has a scientifically unsupported theoretical base and uses diagnostic criteria or symptom lists markedly different from criteria under ICD-10 or DSM-IV-TR, or to attachment behaviors.
In the same year Jabs et al. reported a family that over two generations had granulomatous synovitis, uveitis and cranial neuropathies. The condition was transmitted in an autosomal dominant fashion.Then in 1990 Pastores et al. reported a kindred with a phenotype very similar to what Blau described and suggested that the condition be called Blau Syndrome (BS). They also pointed out the similarities in the families noted above to BS but also pointed out the significant differences in the phenotypes.In 1996 Tromp et al. conducted a genome wide search using affected and non affected members of the original family. A marker, D16S298, gave a maximum logarithm of odds (LOD) score of 3.75 and put the BS susceptibility locus within the 16p12-q21 interval. Hugot et al. found a susceptibility locus for Crohn disease, a granulomatous inflammation of the bowel, on chromosome 16 close to the locus for BS. Based on the above information Blau suggested in 1998 that the genetic defect in BS and Crohn Disease might be the same or similar. Finally in 2001 Miceli-Richard et al. found the defect in BS to be in the nucleotide-binding domain of CARD15/NOD2. They commented in their article that mutations in CARD15 had also been found in Crohns disease. Confirmation of the defect in BS being in the CARD15 gene was made by Wang et al. in 2002 using the BS family and others.