DI may be treated with a medication called desmopressin acetate (DDAVP).Oxytocin is also produced in the posterior pituitary gland. Though best known for its role in childbirth and lactation, oxytocin has also been found to have a role in human bonding, increase in trust, and decrease in fear. Hypothalamic dysfunction may also result in problems with feeding, sleep, and body temperature regulation. Feeding behaviors in children with ONH often include hyperphagia (overeating), resulting in obesity; or hypophagia (reduced food intake) with or without weight loss. Children also frequently experience aversion to specific textures of food. Disturbance of circadian sleep rhythm, resulting in abnormal sleep-wake cycles, is noted in one-third of children with ONH. This disturbance could result in behavioral problems and disruption of family life. Development
More than 70% of children with ONH experience developmental delay, ranging from isolated focal defects to delay in all areas of development (global delay). Motor delay is most common (75%) and communication delay is least common (44%). Predictors of significantly delayed development include hypoplasia or agenesis of the corpus callosum and hypothyroidism. The absence of the septum pellucidum does not predict developmental delay. Delays may occur in unilateral (39%) as well as bilateral (78%) cases. Cause
Genetic risks
Mutations of genes involved in transcription regulation, chromatin remodelling, α-dystroglycan glycosylation, cytoskeleton and scaffolding protein, RNA splicing, and the MAP kinase signalling pathway are currently known to cause ONH.
Chemotherapy is broken down into 2 phases:

Induction therapy: first short and invasive phase of treatment with the goal to the blood of blasts and reduce the number of blasts in the bone marrow back to normal. Consolidation therapy: second phase given in cycles that occur after the patient has recovered from induction therapy. Its objective is to kill remaining blasts that cant be seen.In some cases, an allogenic bone marrow transplantation can be performed. If AML with chromosomal abnormalities such as inv(16) are often cured by the standard chemotherapy regimen. Prognosis
With AMML being difficult to fully treat, the five-year survival rate is about 38-72% which typically decrease to 35-60% if theres no bone marrow transplantation performed. Generally older patients over 60 have a poor outlook due to prior health status before the diagnosis and the aggressive chemotherapy regimen used. The aggressive chemotherapy regimen can lead to long-term side effects such as prolonged anemia, leukocytopenia, neutropenia, and thrombocytopenia. The use of anthracycline drugs can cause a decrease in cardiac contractility, both short and long term. Those with AML-M4 inv(16) have a favorable prognosis with a five-year overall survival rate of 61%. Epidemiology
AML is commonly seen in pediatric patients with higher pediatric incidence in Hispanics and Asians as compared to non-Hispanic Caucasian and African Americans in the USA. Predisposition to AML includes but not limited to:Down syndrome, Klinefelters syndrome, and Fanconis anemia. Acquired predisposing factors include: aplastic anemia, chemotherapy, prenatal exposure to tobacco, marihuana, and alcohol.