The current first choice is generally octreotide or lanreotide; however, bromocriptine and cabergoline are both cheaper and easier to administer. With all of these medications, long-term therapy is necessary, because their withdrawal can lead to rising GH levels and tumor re-expansion.Radiation therapy is generally used for people whose tumors are not completely removed by surgery, for people who are not good candidates for surgery because of other health problems, and for people who do not respond adequately to surgery and medication. Prognosis
Life expectancy of people with acromegaly is dependent on how early the disease is detected. Life expectancy after the successful treatment of early disease is equal to that of the general population. Acromegaly can often go on for years before diagnosis, resulting in poorer outcome, and it is suggested that the better the growth hormone is controlled, the better the outcome. Upon successful surgical treatment, headaches and visual symptoms tend to resolve. One exception is sleep apnea, which is present in around 70% of cases, but does not tend to resolve with successful treatment of growth hormone level. While hypertension is a complication of 40% of cases, it typically responds well to regular regimens of blood pressure medication. Diabetes that occurs with acromegaly is treated with the typical medications, but successful lowering of growth hormone levels often alleviates symptoms of diabetes. Hypogonadism without gonad destruction is reversible with treatment. Acromegaly is associated with a slightly elevated risk of cancer. Notable people
Famous people with acromegaly include:

Daniel Cajanus (1704–1749), "The Finnish Goliath".
Some acquired conditions may share some features with EME and should be differentiated from it. These include hypoxic-ischaemic encephalopathy, central nervous system infections, acute metabolic disturbances or acute vascular events. Mechanism
Pathology results in EME consist of multifocal changes in white matter, imperfect lamination of the deep cortical layers, astrocytic proliferation, and demyelination. Diagnosis
Electroencephalogram (EEG) is usually characterized by a burst suppression pattern. Subsequently it may transition to hypsarrhythmia, a chaotic pattern on EEG, or other severely abnormal EEG patterns. Neuroimaging is useful in assessing a possible underlying structural causality that might cause EME. MRI findings depend on the underlying etiology and may be normal or not at diagnosis. Prevention
Early identification of metabolism error defects is very essential in prevention as the traditional antiepileptic drug are usually not very effective, proper treatment aiming to the conditions can prevent neurological worsening. Genetic counselling is critical given the high prevalence of genetic mutations and early genetic testing also helps to avoid unnecessary procedures and unsuccessful treatment. The families who are at risk, prophylactic treatment is suggested as it may stop the seizure and help in recovering the neurodevelopmental consequences. Management
Antiepileptic drugs are used to treat EME, but it is difficult to control seizures with anti-epileptic drugs alone. Phenobarbital, valproate, pyridoxine, zonisamide, and benzodiazepines have all been used but with inadequate usefulness in seizure control. Some patients show favorable response to sodium channel agents, often at high dose. There are various means to add on the treatment when seizures are resistant. A ketogenic diet can be useful in controlling seizures.