In those who are asymptomatic or without obvious causes of hyperprolactinemia, macroprolactin should be assessed and ruled out. Treatment
Treatment for hyperprolactinemia is usually dependent upon its cause, ranging from hypothyroidism, drug-induced hyperprolactinemia, hypothalamic disease, idiopathic hyperprolactinemia, macroprolactin, or prolactinoma. Therefore, in order to provide the proper management of hyperprolactinemia, the pathological form and physiological increase in prolactin levels are differentiated, and the correct cause of hyperprolactinemia must be identified before treatment. For functional asymptomatic hyperprolactinemia, the treatment of choice is removing the associated cause, including antipsychotic therapy. However, prolactin levels should be drawn and monitored both prior to any discontinuation or changes to therapy, and afterwards. With symptomatic hyperprolactinemia, stopping antipsychotic drugs for a short trial period are not recommended due to the risk of exacerbation or relapse of symptoms. Options for treatment include decreasing the dose of antipsychotics, adding aripiprazole as an adjunctive therapy, and switching antipsychotics as a last resort. In pharmacologic hyperprolactinemia, the concerning drug can be switched to another treatment or discontinued entirely. Vitex agnus-castus extract may be tried in cases of mild hyperprolactinemia. No treatment is required in asymptomatic macroprolactin and instead, serial prolactin measurements and pituitary imaging is monitored in a regular follow-up appointments.Medical therapy is the preferred treatment in prolactinomas. In most cases, medications that are dopamine agonists, such as cabergoline and bromocriptine (often preferred when pregnancy is possible), are the treatment of choice used to decrease prolactin levels and tumor size upon the presence of microadenomas or macroadenomas.
Prognosis
In infants, germinal matrix haemorrhage is associated with cerebral palsy, problems with cognition, and hydrocephalus. With improved technological advances in science and medicine, survival for preterm infants with this type of neurological disorder has improved and less preterm infants with germinal matrix haemorrhage have severe cerebral palsy. An estimated 15% of preterm infants who survive develop cerebral palsy and 27% of the infants who survive experience moderate to severe neurosensory deficits by the time they reach 18–24 months old.Prognosis is very poor when IVH results from intracerebral hemorrhage related to high blood pressure and is even worse when hydrocephalus follows. It can result in dangerous increases in ICP and can cause potentially fatal brain herniation. Even independently, IVH can cause morbidity and mortality. First, intraventricular blood can lead to a clot in the CSF conduits blocking its flow and leading to obstructive hydrocephalus which may quickly result in increased intracranial pressure and death. Second, the breakdown products from the blood clot may generate an inflammatory response that damages the arachnoid granulations, inhibiting the regular reabsorption of CSF and resulting in permanent communicating hydrocephalus. Associated conditions
Brain contusions and subarachnoid hemorrhages are commonly associated with IVH. The bleeding can involve the anterior communicating artery or the posterior communicating artery. In both adults and infants, IVH can cause dangerous increases in ICP, damage to the brain tissue, and hydrocephalus. Epidemiology
IVH has been reported to occur in approximately 25% of infants who are born with a very low birth weight.