Physical, occupational, and speech therapies along with special education techniques can stimulate children with idic(15) to develop to their full potential.In terms of medical management of the symptoms associated with Chromosome 15q11.2-q13.1 Duplication Syndrome, families should be aware that individuals with chromosome 15 duplications may tolerate medications differently and may be more sensitive to side effects for some classes of medications, such as the serotonin reuptake inhibitor type medications (SSRI). Thus, these should be used with caution and any new medication should be instituted in a controlled setting, with slow titration of levels and with a clear endpoint as to what the expected outcome for treatment is.There is an increased risk of sudden, unexpected death among children and adults with this syndrome. The full cause is not yet understood but it is generally attributed to SUDEP (Sudden Unexplained Death in Epilepsy). Epidemiology
About half of all marker chromosomes are idic(15) but idic(15) in itself is one of the rare chromosome abnormalities. Incidence at birth appears to be 1 in 30,000 with a sex ratio of almost 1:1; however, since dysmorphic features are absent or subtle and major malformations are rare, chromosome analysis may not be thought to be indicated, and some individuals, particularly in the older age groups, probably remain undiagnosed. There are organizations for families with idic(15) children that offer extensive information and support. Research
Patients with idic(15) and int dup(15) often feature a distinctive electroencephalography (EEG) signature or biomarker in the form of high amplitude spontaneous beta frequency (12–30 Hz) oscillations.
This EEG signature was first noted as a qualitative pattern in clinical EEG readings and was later described quantitatively  by researchers at the University of California, Los Angeles and their collaborators within the network of national Dup15q clinics. This group of researchers found that beta activity in children with Dup15q syndrome is significantly greater than that observed in (1) healthy, typically developing children of the same age and (2) children of the same age and IQ with autism not caused by a known genetic disorder (i.e., nonsyndromic ASD). The EEG signature appears almost identical to beta oscillations induced by benzodiazepine drugs that modulate GABAA receptors, suggesting that the signature is driven by overexpression of duplicated GABAA receptor genes GABRA5, GABRB3, and GABRG3 found on 15q11.2-q13.1. Treatment monitoring and identification of molecular disease mechanisms may be facilitated by this biomarker. See also
marker chromosome 15 syndrome

References


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