Multisystem developmental disorder (MSDD) is a term used by Stanley Greenspan to describe children under age 3 who exhibit signs of impaired communication as in autism, but with strong emotional attachments atypical of autism.[citation needed] It is described in the DC:0-3R manual as an optional diagnosis for children under two years of age.[1][2]
Other uses of the term
The term multisystem developmental disorder has also been used to describe various developmental disorders. These include:
Alagille syndrome,[3] an autosomal dominant disorder with a wide range of features and manifestations. Its five most significant features are chronic cholestasis, a condition where bile cannot flow from the liver to the duodenum, occurring in 95% of cases; heart abnormalities (over 90%); butterfly vertebrae; posterior embryotoxon and a distinctive face (prominent forehead, deep-set eyes, and a pointed chin).[4]
Rubinstein-Taybi syndrome,[5][6] a syndrome characterized by broad thumbs, facial abnormalities, and big toes alongside moderate to severe intellectual disability.[7]
Williams syndrome,[8][9] a neurodevelopmental disorder characterized by a unique profile of strengths and deficits; most with the condition have mild intellectual disability but have grammatical and lexical abilities above what would be expected from their IQs.[10] They are hypersocial and empathetic, but social isolation is commonly experienced.[11]
Proteus syndrome,[12] a congenital disorder causing disproportionate growth of skin, bone, and other tissues.[13]
Asphyxiating thoracic dysplasia,[14] an autosomal recessive skeletal disorder with an estimated prevalence of between 1 in 100,000 and 1 in 130,000 live births.[15]
^Oztop, D; Uslu, R (2007). "Behavioral, interactional and developmental symptomatology in toddlers of depressed mothers: A preliminary clinical study within the DC:0-3 framework". The Turkish Journal of Pediatrics. 49 (2): 171–8. PMID17907517.
^Hendrix, JD Jr; Greer, KE (1996). "Rubinstein-Taybi syndrome with multiple flamboyant keloids". Cutis; Cutaneous Medicine for the Practitioner. 57 (5): 346–8. PMID8726717.
^Rio, T; Urbán, Z; Csiszár, K; Boyd, CD (2008). "A gene-dosage PCR method for the detection of elastin gene deletions in patients with Williams syndrome". Clinical Genetics. 54 (2): 129–35. doi:10.1111/j.1399-0004.1998.tb03715.x. PMID9761391. S2CID12793159.
^Scheiber, D; Fekete, G; Urban, Z; Tarjan, I; et al. (2006). "Echocardiographic findings in patients with Williams-Beuren syndrome". Wiener Klinische Wochenschrift. 118 (17–18): 538–42. doi:10.1007/s00508-006-0658-2. PMID17009066. S2CID41861608.
^Bellugi, U; Wang, PP; Jernigan, TL (1994). "Williams Syndrome: An Unusual Neuropsychological Profile". In Broman, SH; Grafman, J (eds.). Atypical Cognitive Deficits in Developmental Disorders: Implications for Brain Function. Taylor & Francis. pp. 23–56. ISBN978-0-8058-1180-3.
Scheeringa, MS (2001). "The differential diagnosis of impaired reciprocal social interaction in children: A review of disorders". Child Psychiatry and Human Development. 32 (1): 71–89. doi:10.1023/A:1017511714145. PMID11579660. S2CID43311652.
Wieder, S (1996). "Integrated treatment approaches for young children with multisystem developmental disorder". Infants & Young Children. 8 (3): 24–34. doi:10.1097/00001163-199601000-00005. S2CID145177134.