Cognitive behavioral therapy in particular can provide benefits, especially alongside medication, in the treatment of adult ADHD. Epidemiology
In North America and Europe, it is estimated that three to five percent of adults have ADHD. Of those adults with ADHD, an estimated 10% of those have received a formal diagnosis. It has been estimated that 5% of the global population has ADHD (including cases not yet diagnosed). In the context of the World Health Organization World Mental Health Survey Initiative, researchers screened more than 11,000 people aged 18 to 44 years in ten countries in the Americas, Europe and the Middle East. On this basis they estimated the adult ADHD proportion of the population to average 3.5 percent with a range of 1.2 to 7.3 percent, with a significantly lower prevalence in low-income countries (1.9%) compared to high-income countries (4.2%). The researchers concluded that adult ADHD often co-occurs with other disorders, and that it is associated with considerable role disability. Although they found that few adults are treated for ADHD itself, in many instances treatment is given for the co-occurring disorders. History
Early work on disorders of attention was conducted by Alexander Crichton in 1798 writing about "mental restlessness". The underlying condition came to be recognized from the early 1900s by Sir George Still. Efficacy of medications on symptoms was discovered during the 1930s and research continued throughout the twentieth century.
It is possible for a newborn with this disease to have neutropenia and neonatal alloimmune thrombocytopenia as well. Hemolysis leads to elevated bilirubin levels. After delivery, bilirubin is no longer cleared (via the placenta) from the neonates blood and the symptoms of jaundice (yellowish skin and yellow discoloration of the whites of the eyes, or icterus) increase within 24 hours after birth. Like other forms of severe neonatal jaundice, there is the possibility of the neonate developing acute or chronic kernicterus, however the risk of kernicterus in HDN is higher because of the rapid and massive destruction of blood cells. It is important to note that isoimmunization is a risk factor for neurotoxicity and lowers the level at which kernicterus can occur. Untreated profound anemia can cause high-output heart failure, with pallor, enlarged liver and/or spleen, generalized swelling, and respiratory distress.HDN can be the cause of hydrops fetalis, an often-severe form of prenatal heart failure that causes fetal edema. Complications
Complications of HDN could include kernicterus, hepatosplenomegaly, inspissated (thickened or dried) bile syndrome and/or greenish staining of the teeth, hemolytic anemia and damage to the liver due to excess bilirubin. Conditions that may cause similar symptoms in the newborn period include: acquired hemolytic anemia, congenital toxoplasma, congenital syphilis infection, congenital obstruction of the bile duct, and cytomegalovirus (CMV) infection. High at birth or rapidly rising bilirubin
Prolonged hyperbilirubinemia
Bilirubin Induced Neurological Dysfunction
Cerebral Palsy
Kernicterus
Neutropenia
Thrombocytopenia
Hemolytic anemia – must not be treated with iron
Late onset anemia – must not be treated with iron. Can persist up to 12 weeks after birth.