At the present time, there is no specific treatment that can undo any chromosomal abnormality, nor the genetic pattern seen in people with idic(15). The extra chromosomal material in those affected was present at or shortly after conception, and its effects on brain development began taking place long before the child was born. Therapies are available to help address many of the symptoms associated with idic(15). 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).

Both patients with idic(15) and int dup(15) (together, Dup15q syndrome) 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 GABA receptors, suggesting that the signature is driven by overexpression of duplicated GABA 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.

Potocki–Lupski syndrome (PTLS), also known as dup(17)p11.2p11.2 syndrome, trisomy 17p11.2 or duplication 17p11.2 syndrome, is a contiguous gene syndrome involving the microduplication of band 11.2 on the short arm of human chromosome 17 (17p11.2). The duplication was first described as a case study in 1996. In 2000, the first study of the disease was released, and in 2007, enough patients had been gathered to complete a comprehensive study and give it a detailed clinical description. PTLS is named for two researchers involved in the latter phases, Drs. Lorraine Potocki and James R. Lupski of Baylor College of Medicine.

PTLS was the first predicted of a homologous recombination (microdeletion or microduplication) where both reciprocal recombinations result in a contiguous gene syndrome. Its reciprocal disease is Smith–Magenis syndrome (SMS), in which the chromosome portion duplicated in PTLS is deleted altogether.

Potocki–Lupski syndrome is considered a rare disease, predicted to appear in at least 1 in 20,000 humans.

Symptoms of the syndrome include intellectual disability, autism, and other disorders unrelated to the listed symptoms.

The duplication involved in PTLS is usually large enough to be detected through G-banding alone, though there is a high false negative rate. To ascertain the diagnosis when karyotyping results are unclear or negative, more sophisticated techniques such as subtelomeric fluorescent in-situ hybridization analysis and array comparative genomic hybridization (aCGH) may be used.

There have been no major breakthroughs in the treatment of PKAN, with most pharmacologic treatments focusing on the easing or temporary relieving of PKAN’s symptoms. Iron chelating agents have been used somewhat successfully in retarding the disorder, but they have not been a significant success.

Current research focuses on the future use of high dose pantothenate, the PANK2 enzyme substrate, in possibly alleviating symptoms as well as the further development of iron chelating agents that may be better aimed at reaching the central nervous system and working to better remove excess iron from the individual’s system.

Complications may result from the medication used to treat symptoms. Immobility from the disease can also lead to skin breakdown, respiratory infections, and blood clots, among others.

Survival rates for those diagnosed with typical PKAN is 11.18 years with a standard deviation of 7.8 years.

For those whose RLS disrupts or prevents sleep or regular daily activities, medication may be useful. Evidence supports the use of dopamine agonists including: pramipexole, ropinirole, rotigotine, and cabergoline. They reduce symptoms, improve sleep quality and quality of life. Levodopa is also effective. One review found pramipexole to be better than ropinirole.

There are, however, issues with the use of dopamine agonists including augmentation. This is a medical condition where the drug itself causes symptoms to increase in severity and/or occur earlier in the day. Dopamine agonists may also cause rebound when symptoms increase as the drug wears off. In many cases, the longer dopamine agonists have been used the higher the risk of augmentation and rebound as well as the severity of the symptoms. Also, a recent study indicated that dopamine agonists used in restless leg syndrome can lead to an increase in compulsive gambling.

- Gabapentin or pregabalin, a non-dopaminergic treatment for moderate to severe primary RLS

- Opioids are only indicated in severe cases that do not respond to other measures due to their high rate of side effects.

Benzodiazepines, such as diazepam or clonazepam, are not generally recommended, and their effectiveness is unknown. They however are sometimes still used as a second line, as add on agents. Quinine is not recommended due to its risk of serious side effects involving the blood.

Treatment of restless legs syndrome involves identifying the cause of symptoms when possible. The treatment process is designed to reduce symptoms, including decreasing the number of nights with RLS symptoms, the severity of RLS symptoms and nighttime awakenings. Improving the quality of life is another goal in treatment. This means improving overall quality of life, decreasing daytime sleepiness, and improving the quality of sleep. Pharmacologic treatment involves dopamine agonists or gabapentin enacarbil as first line drugs for daily restless legs syndrome, and opioids for treatment of resistant cases. RLS drug therapy is not curative and has side effects such as nausea, dizziness, hallucinations, orthostatic hypotension, or daytime sleep attacks. An algorithm created by Mayo Clinic researchers provides guidance to the treating physician and patient, including non-pharmacological and pharmacological treatments.

Treatment of RLS should not be considered until possible medical causes are ruled out, especially venous disorders. Secondary RLS may be cured if precipitating medical conditions (anemia, venous disorder) are managed effectively. Secondary conditions causing RLS include iron deficiency, varicose veins, and thyroid problems.