Disorganized schizophrenia, or hebephrenia, was a subtype of schizophrenia prior to 2013. Subtypes of schizophrenia were no longer recognized as separate conditions in the DSM 5, published in 2013. The disorder is no longer listed in the 11th revision of the International Classification of Diseases (ICD-11). Disorganized schizophrenia was classified within ICD-10 the existing classification, in practice, until January 1,  2022, as a mental and behavioural disorder,  because the classification was thought to be an extreme expression of the disorganization syndrome that has been hypothesized to be one aspect of a three-factor model of symptoms in schizophrenia, the other factors being reality distortion (involving delusions and hallucinations) and psychomotor poverty (lack of speech, lack of spontaneous movement and various aspects of blunting of emotion). Presentation
The condition is also known as hebephrenia, named after the Greek term for "adolescence" – ἥβη (hḗbē) – and possibly the ancient-Greek goddess of youth, Hebe, daughter of Hera. The term refers to the ostensibly more prominent appearance of the disorder in persons around puberty.The prominent characteristics of this form are disorganized behavior and speech (see formal thought disorder), including loosened associations and schizophasia ("word salad"), and flat or inappropriate affect. In addition, psychiatrists must rule out any possible sign of catatonic schizophrenia. The most prominent features of disorganized schizophrenia are not delusions and hallucinations, as in paranoid schizophrenia, although fragmentary delusions (unsystemized and often hypochondriacal) and hallucinations may be present.
This test was not universally effective, as it had both false negative and false positive results.Ornithine transcarbamylase is only expressed in the liver, thus performing an enzyme assay to confirm the diagnosis requires a liver biopsy. Before molecular genetic testing was commonly available, this was one of the only methods for confirmation of a suspected diagnosis. In cases where prenatal diagnosis was requested, a fetal liver biopsy used to be required to confirm if a fetus was affected. Modern molecular techniques have eliminated this need, and gene sequencing is now the preferred method of diagnosis in asymptomatic family members after the diagnosis has been confirmed in a proband. Treatment
The treatment goal for individuals affected with OTC deficiency is the avoidance of hyperammonemia. This can be accomplished through a strictly controlled low-protein diet, as well as preventative treatment with nitrogen scavenging agents such as sodium benzoate. The goal is to minimize the nitrogen intake while allowing waste nitrogen to be excreted by alternate pathways. Arginine is typically supplemented as well, in an effort to improve the overall function of the urea cycle. If a hyperammonemic episode occurs, the aim of treatment is to reduce the individuals ammonia levels as soon as possible. In extreme cases, this can involve hemodialysis.Gene therapy had been considered a possibility for curative treatment for OTC deficiency, and clinical trials were taking place at the University of Pennsylvania in the late 1990s.