eMedicine Specialties > Oncology > Carcinomas of the Central and Peripheral Nervous System

Astrocytoma: Treatment & Medication

Author: Benjamin Kennedy,, Columbia University College of Physicians and Surgeons
Coauthor(s): Jeffrey N Bruce, MD, Edgar M Housepian Professor of Neurological Surgery Research, Professor of Neurological Surgery, Director of Brain Tumor Tissue Bank, Director of Bartoli Brain Tumor Laboratory, Department of Neurosurgery, Columbia University College of Physicians and Surgeons
Contributor Information and Disclosures

Updated: Jan 23, 2009

Treatment

Medical Care

Generally, care of patients with brain tumors is primarily directed by a neurologist or specialist in neurooncology. There is no accepted standard of treatment for low-grade or anaplastic astrocytoma. Decisions on operative intervention and the use of chemotherapy and radiation therapy are generally best made by a team approach, including input from the involved neurosurgeon, radiation oncologist, and medical oncologist or neurologist.

  • Typically, anaplastic astrocytomas are treated with surgery, radiotherapy, and adjuvant temozolomide. Some practitioners add concomitant temozolomide, though no data from controlled trials exist to support concomitant temozolomide.15,16
  • Anaplastic astrocytomas are usually more responsive to chemotherapy than glioblastomas.17,18 For recurrent anaplastic astrocytomas previously treated with nitrosoureas, temozolomide showed a 35% response rate, and compared to therapies with lower response rates, temozolomide provided an increased 6-month survival rate (46% vs 31%).19,20 Some smaller survival benefit has been shown with adjuvant BCNU.21
  • Treatment of low-grade astrocytomas remains more controversial. The role of maximal surgical resection, timing of radiotherapy, and the role, timing, and appropriate agents of chemotherapy are not clear. The controversy due to a lack of strong data is compounded by the relatively young age of the patients, the relatively indolent natural history of low-grade astrocytomas, and the morbidity associated with these interventions.22
  • Patients with an astrocytoma and a history of seizures should receive anticonvulsant therapy with monitoring of the drug concentration in the blood stream. The use of anticonvulsants prophylactically in astrocytoma patients with no prior history of seizures has been reported but remains controversial.
  • The use of corticosteroids, such as dexamethasone, yields rapid improvement in most patients secondary to a reduction of tumor mass effect. Concurrent prophylaxis for gastrointestinal ulcers should be prescribed with corticosteroid administration.
  • Brainstem gliomas: Brainstem tumors account for 10-20%23 of all CNS tumors in the pediatric population, typically diagnosed between ages 7-9.24,25 Though many classification schemes exist, treatment and prognosis for brainstem gliomas typically depends on whether the tumor is diffuse or focal.
  • Diffuse brainstem gliomas make up 58-75%26 of all brainstem tumors, typically arise in the pons, and are noncircumscribed on MRI. They are often malignant fibrillary astrocytomas (WHO grade III or IV), which infiltrate along white matter tracts into the midbrain and thalamus and have a rapidly progressive and fatal course.
    • Clinical presentation of these tumors often involves ataxia, cerebellar signs, and long tract signs.27 When clinical and radiographic evidence suggests diffuse brainstem glioma, biopsy is of limited use as tumor histology does not frequently alter treatment.26,28,29,30,31,32,33,34
    • No benefit of surgical resection has been shown, largely due to the eloquence of the region and diffuse and aggressive nature of the tumor.27,35 Corticosteroids may provide temporary benefit by reduction of edema. Irradiation has been shown to provide temporary clinical improvement and is sometimes employed, but a large phase III trial showed no benefit.36 Even with radiation therapy, 1-year survival has been shown to be 35-46%, and 3-year survival 11-17%.37,38 Chemotherapy is also sometimes used.39 No treatment, however, has been shown to cure or prolong survival in these patients, and radiation necrosis and chemotherapy side effects can be significant. Convection-enhanced delivery of chemotherapy offers one potential avenue for improving the prognosis of these patients, and studies are ongoing.
  • Focal brainstem gliomas are usually WHO grade I or II, well-circumscribed on MRI with variable contrast enhancement, are more often found in the medulla and midbrain and have a much better prognosis than diffuse brainstem gliomas. Surgery is often the primary treatment for focal brainstem gliomas as well as dorsal exophytic brainstem gliomas, though the decision to operate, surgical approach, and extent of resection depend on location, patient factors, and the surgeon's judgment. Obstructive hydrocephalus is common, usually treated by a separate procedure, either endoscopic third ventriculostomy or shunt placement.40

Surgical Care

The roles of surgery in the patient with astrocytoma are (1) to remove or debulk the tumor and (2) to provide tissue for histological diagnosis, permitting tailoring of adjuvant therapy and assessment of prognosis.41 A stereotactic biopsy is a safe and simple method for establishing a tissue diagnosis. The use of stereotactic biopsy can be limited by sampling error and the risk of biopsy-induced intracerebral hemorrhage. Diversion of CSF by external ventricular drain (EVD) or ventriculoperitoneal shunt (VPS) may be required to decrease ICP as part of nonoperative management or prior to definitive surgical therapy if hydrocephalus is present.

Total resection of astrocytoma is often impossible because the tumors often invade into eloquent regions of the brain and exhibit tumor infiltration that is only detectable on a microscopic scale. Therefore, surgical resection only provides for improved survival advantage and histological diagnosis of the tumor rather than offering a cure. However, craniotomy for tumor resection can be performed safely and is generally undertaken with the intent to cause the least possible neurological injury to the patient. Complete resection (>98% based on volumetric MRI) has been shown to improve median survival compared with subtotal resection (13 vs 8.8 mo).42

Consultations

  • A neurologist should be consulted to document a patient's detailed neurological examination. This establishes a baseline and partly assesses the possibility of occult disease. Employing multiple modalities, the neurologist must correlate symptomatology with anatomic and functional imaging. This physician also may manage antiepileptic medication for patients manifesting seizures.
  • A neurosurgeon should be consulted to assess the risks and benefits of surgical resection, stereotactic biopsy, stereotactic radiosurgery, and CSF diversion.
  • A neurooncologist may be consulted to help coordinate a comprehensive therapeutic plan. Once a histological diagnosis is determined, the neurooncologist should be consulted to provide comprehensive adjunctive therapy, including the use of chemotherapy and radiation.

Activity

  • No broad restrictions on activity are prescribed, other than those dictated by the nature and the extent of neurological symptoms and disability.
  • Seizures, if uncontrolled, may preclude driving.
  • Physical and occupational therapy may be required for recovery of full or partial function.

Medication

No specific drug treatment exists for low-grade glioma. Certain conditions (eg, low-grade astrocytoma) typically require treatment. For seizures, the patient is usually started on levetiracetam (Keppra), phenytoin (Dilantin), or carbamazepine (Tegretol). Levetiracetam is often used because it lacks the effects on the P450 system seen with phenytoin and carbamazepine, which can interfere with antineoplastic therapy. Steroid therapy, usually combined with gastroprotectant, is initiated for vasogenic edema around tumor.

Anticonvulsants

These agents prevent seizure recurrence and terminate clinical and electrical seizure activity.


Levetiracetam (Keppra)

Used as adjunct therapy for partial seizures and myoclonic seizures. Also indicated for primary generalized tonic-clonic seizures. Mechanism of action is unknown.

Adult

1000 mg/d PO divided bid (500 mg bid); may increase by 1000 mg/d increments q2wk; not to exceed 3000 mg/d; long-term experience at doses >3000 mg/d is relatively minimal, and there is no evidence that doses >3000 mg/d offer additional benefit

Pediatric

Partial onset seizures:
<4 years: Not established
4-15 years: 20 mg/kg/d PO divided bid; may increase by 20 mg/kg/d increments q2wk; not to exceed 60 mg/kg/d; use oral solution if weight <20 kg
>15 years: Administer as in adults
Myoclonic seizures:
<12 years: Not established
>12 years: Administer as in adults
Tonic-clonic seizures:
<6 years: Not established
6-15 years: 10 mg/kg PO bid; may increase daily dose by 20-mg/kg increments q2wk, not to exceed 30 mg/kg bid
>15 years: Administer as in adults

None reported; does not inhibit CYP450 isoenzymes, epoxide hydrolase, or UDP-glucuronidation; probenecid inhibits renal clearance of ucb L057 (inactive levetiracetam metabolite)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal impairment (reduce dose); major side effects include somnolence, asthenia, incoordination, mild leukopenia (3%) and behavioral changes such as anxiety, hostility, emotional lability, depression and psychosis (1-2%), and depersonalization; seizure frequency may increase following discontinuing drug (discontinue gradually); statistically significant decreases in RBCs and WBCs have been observed


Phenytoin (Dilantin)

Effective in partial and generalized tonic-clonic seizures. Blocks sodium channel and prevents repetitive firing of action potentials.

Adult

Loading dose: 15 mg/kg (1000 mg) PO/IV over 4 h divided into 2 or 3 doses
Maintenance dose: 5 mg/kg/d (300 mg) PO/IV qd or divided tid, usually adjusted based on serum levels

Pediatric

Loading dose: 15 mg/kg PO/IV over 4 h divided bid/tid
Maintenance dose: 5 mg/kg/d PO/IV frequently divided tid, usually adjusted based on serum levels

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid

Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform blood counts and urinalyses when beginning therapy and at monthly intervals for several months thereafter to monitor for blood dyscrasias; discontinue use if a skin rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugars); discontinue use if hepatic dysfunction occurs; monitor for nystagmus, ataxia, and diplopia


Carbamazepine (Tegretol)

Similar to phenytoin. Effective in partial and generalized tonic-clonic seizures. Blocks sodium channel and prevents repetitive firing of action potentials.

Adult

200-600 mg PO tid/qid (bid with ER); monitor serum levels, maintain in 4- to 8-mcg/mL range

Pediatric

15-25 mg/kg/d PO divided tid/qid (bid with ER)

Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; carbamazepine may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels); increases metabolism of warfarin, valproic acid, and phenytoin

Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not use to relieve minor aches or pains; caution with increased intraocular pressure; obtain CBCs and serum-iron baseline before treatment, during first 2 mo, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; occasional leukopenia (aplastic anemia) is more common in elderly persons

Corticosteroids

These drugs reduce edema around the tumor, frequently leading to symptomatic and objective improvement.


Dexamethasone (Decadron, AK-Dex, Alba-Dex, Dexone, Baldex)

Postulated mechanisms of action in brain tumors include reduction in vascular permeability, cytotoxic effects on tumors, inhibition of tumor formation, and decreased CSF production.

Adult

Significant peritumoral edema: 16 mg/d PO/IV divided q6h, continue until improvement then taper to termination or minimum effective dose

Pediatric

0.15 mg/kg/d PO/IV divided q6h

Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization

Documented hypersensitivity; active bacterial or fungal infection

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; possible complications include hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections; severe stress may require increasing dose; iatrogenic Cushing syndrome (acne, hirsutism, and facial plethora) may occur

Antineoplastic Agent, Alkylating Agent

These agents inhibit cell growth and proliferation.


Temozolomide (Temodar)

Oral alkylating agent converted to MTIC at physiologic pH; 100% bioavailable; approximately 35% crosses the blood-brain barrier.

Adult

150 mg/m2 PO qd for 5 consecutive d per 28-d cycle; adjust dose each cycle according to neutrophil and platelet nadir during previous cycle and current counts

Pediatric

Not established

Documented hypersensitivity to temozolomide or DTIC, since each drug is metabolized to MTIC

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Causes bone marrow suppression resulting in thrombocytopenia, anemia, and leukopenia (check blood counts weekly during concomitant phase, then at day 1 and 21 of each cycle); common adverse effects include nausea, vomiting, and alopecia; it is not known if the drug is excreted in breast milk and because of potential serious adverse effects in infants, breastfeeding should be discontinued; PCP prophylaxis required during concomitant phase, continue if lymphocytopenia develops

More on Astrocytoma

Overview: Astrocytoma
Differential Diagnoses & Workup: Astrocytoma
Treatment & Medication: Astrocytoma
Follow-up: Astrocytoma
Multimedia: Astrocytoma
References
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Further Reading

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Keywords

low-grade astrocytoma, fibrillary astrocytoma, gemistocytic astrocytoma, protoplasmic astrocytoma, diffuse astrocytoma, pilocytic astrocytoma, pilocystic astrocytoma, juvenile pilocytic astrocytoma, anaplastic astrocytoma, glioblastoma multiforme, CNS neoplasm, CNS cancer, CNS malignancy, immortalized astrocyte

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Contributor Information and Disclosures

Author

Benjamin Kennedy,, Columbia University College of Physicians and Surgeons
Disclosure: Nothing to disclose.

Coauthor(s)

Jeffrey N Bruce, MD, Edgar M Housepian Professor of Neurological Surgery Research, Professor of Neurological Surgery, Director of Brain Tumor Tissue Bank, Director of Bartoli Brain Tumor Laboratory, Department of Neurosurgery, Columbia University College of Physicians and Surgeons
Jeffrey N Bruce, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Neurological Surgeons, Congress of Neurological Surgeons, New York Academy of Sciences, North American Skull Base Society, Society for Neuro-Oncology, and Southwest Oncology Group
Disclosure: NIH Grant/research funds Other

Medical Editor

Robert C Shepard, MD, FACP, Associate Professor of Medicine in Hematology and Oncology at University of North Carolina at Chapel Hill; Vice President of Scientific Affairs, Therapeutic Expertise, Oncology, at PRA International
Robert C Shepard, MD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physician Executives, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Medical Association, American Medical Informatics Association, American Society of Hematology, Association of Clinical Research Professionals, Eastern Cooperative Oncology Group, European Society for Medical Oncology, Massachusetts Medical Society, and Society for Biological Therapy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

Rajalaxmi McKenna, MD, FACP, Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD, Clinical Professor of Medicine, Division of Hematology/Medical Oncology, Department of Internal Medicine, University of Arizona College of Medicine at Tucson; Consulting Staff, Arizona Cancer Center
Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research
Disclosure: GlobeImmune Salary Consulting; Amplimed Consulting fee Consulting; FibroGen Consulting fee Consulting

 
 
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