Myxoid foci and oligodendroglioma-like cells may also be present, though these are not specific to pilocytic astrocytoma. Long-standing lesions may show hemosiderin-laden macrophages and calcifications. Treatment
The most common form of treatment is having the tumor surgically removed. Complete removal of the tumor will generally allow functional survival for many years. In particular for pilocytic astrocytomas (commonly indolent masses that may permit normal neurologic function), surgeons may decide to monitor the neoplasms evolution and postpone surgical intervention for some time. However, total resection is often not possible. The location could prohibit access to the neoplasm and lead to incomplete or no resection at all. Left unattended, these tumors may eventually lead to further symptoms due to continued slow growth. Extremely rarely, they may also undergo malignant transformation. If surgery is not possible, recommendations such as chemotherapy or radiation may be suggested. However, side effects from these treatments can be extensive and long term, resulting in some cases in life-long difficulties. Side effects
After treatment, children with pilocytic astrocytoma may experience an improvement of symptoms related to the tumor itself depending on the location, but may also experience side effects related to the treatment:

Symptoms related to increased pressure in the brain often disappear after surgical removal of the tumor. Effects on coordination and balance may improve and might progressively (to completely) disappear as recovery progresses. Steroid treatment is often used to control tissue swelling that may occur pre-and post-operatively. Patients can, however, also develop long-term side effects due to the type of treatment they may receive.
Only its use in rheumatoid arthritis requires the concomitant use of methotrexate by the U.S. Food and Drug Administration (FDA) product labeling; however, the concomitant use of methotrexate in other disease states may help to reduce the bodys immune response to the infliximab and increase its duration of efficacy. Pharmacology
Infliximab is a purified, recombinant DNA-derived chimeric human-mouse IgG monoclonal antibody that consists of mouse heavy and light chain variable regions combined with human heavy and light chain constant regions. It has a serum half-life of 9.5 days and can be detected in serum 8 weeks after infusion treatment.Infliximab neutralizes the biological activity of TNF-α by binding with high affinity to the soluble (free floating in the blood) and transmembrane (located on the outer membranes of T cells and similar immune cells) forms of TNF-α, and inhibits or prevents the effective binding of TNF-α with its receptors. Infliximab and adalimumab (another TNF antagonist) are in the subclass of "anti-TNF antibodies" (they are in the form of naturally occurring antibodies), and are capable of neutralizing all forms (extracellular-, transmembrane-, and receptor-bound) of TNF-α. Etanercept, a third TNF antagonist, is in a different subclass (receptor-construct fusion protein), and, because of its modified form, cannot neutralize receptor-bound TNF-α. Additionally, the anti-TNF antibodies adalimumab and infliximab have the capability of lysing cells involved in the inflammatory process, whereas the receptor fusion protein apparently lacks this capability. Although the clinical significance of these differences have not been absolutely proven, etanercept, has been shown to perform worse than placebo for Crohns disease.