Astrocytoma Clinical Presentation

  • Author: Benjamin Kennedy; Chief Editor: Jules E Harris, MD   more...
 
Updated: Jan 17, 2012
 

History

The type of neurological symptoms that result from astrocytoma development depends foremost on the site and extent of tumor growth in the CNS. Reports of altered mental status, cognitive impairment, headaches, visual disturbances, motor impairment, seizures, sensory anomalies, or ataxia in the patient's history should alert the clinician to the presence of a neurological disorder and should indicate a requirement for further studies. In this event, radiographic imaging, such as CT scan and MRI (with and without contrast), is indicated. Astrocytomas of the spinal cord or brainstem are less common and present with motor/sensory or cranial nerve deficits referable to the tumor's location.

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Physical

  • A detailed neurological examination is required for the proper evaluation of any patient with an astrocytoma. Because these tumors may affect any part of the CNS, including the spinal cord, and may spread to distant regions of the CNS, a thorough physical examination referable to the entire neuraxis is necessary to define the location and extent of disease.
  • Special attention should be paid to signs of increased ICP, such as headache, nausea and vomiting, decreased alertness, cognitive impairment, papilledema, or ataxia, to determine the likelihood of mass effect, hydrocephalus, and herniation risk. Localizing and lateralizing signs, including cranial nerve palsies, hemiparesis, sensory levels, alteration of deep tendon reflexes (DTRs), and the presence of pathological reflexes (eg, Hoffman and Babinski signs), should be noted. Once neurological abnormalities are identified, imaging studies should be sought for further evaluation.
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Causes

  • The etiology of diffuse astrocytomas has been the subject of analytic epidemiological studies that have yielded associations with various disorders and exposures.[6] With the exception of therapeutic irradiation[7] and, perhaps, nitroso compounds (eg, nitrosourea), the identification of specific causal environmental exposures or agents has been unsuccessful. Although some concern has been raised regarding cell phone use as a potential risk factor for development of gliomas, the largest studies have not supported this.[8, 9, 10, 11, 12]
  • Children receiving prophylactic irradiation for acute lymphatic leukemia (ALL), for example, have a 22-fold increased risk of developing CNS neoplasms in WHO grade II, III, and IV astrocytomas, with an interval for onset of 5-10 years. Furthermore, irradiation of pituitary adenomas has been demonstrated to carry a 16-fold increased risk of glioma formation.[13]
  • Evidence exists for genetic susceptibility to glioma development. For example, familial clustering of astrocytomas is well described in inherited neoplastic syndromes, such as Turcot syndrome, neurofibromatosis type 1 (NF1) syndrome, and p53 germ line mutations (eg, Li-Fraumeni syndrome).
  • Biological investigation has implicated that mutations in specific molecular pathways, such as the p53-MDM2-p21 and p16-p15-CDK4-CDK6-RB pathways, are associated with astrocytoma development and progression. In addition, inherited elements of the immune response known as human leukocyte antigens (HLA) have been both positively and negatively associated with an increased risk for the development of glioblastoma multiforme. Two-thirds of low-grade astrocytomas have p53 mutations.[14]
  • Recently, attempts have been made to determine prognosis and response to various treatment modalities based on the individual pattern of genetic changes in a particular patient. For example, patients with oligodendrogliomas that exhibit chromosomal changes at band 1p19q are known to have improved responses to the procarbazine, CCNU, vincristine (PCV) regimen of chemotherapy. Efforts are underway to identify similar unique susceptibilities associated with other commonly altered genes and proteins in astrocytomas. Other groups are working on developing models that will allow for a more accurate assessment of prognosis based on a combination of molecular profiling of the tumors and clinical characteristics of the patient.[15]
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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, Vice-Chairman and 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: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Neurological Surgeons, American Society of Clinical Oncology, Congress of Neurological Surgeons, New York Academy of Sciences, North American Skull Base Society, Pituitary Society, Society for Neuro-Oncology, and Society of Neurological Surgeons

Disclosure: NIH Grant/research funds Other

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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, Section of Hematology/Oncology, University of Arizona College of Medicine, 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

Additional Contributors

We wish to acknowledge previous contributions to this chapter from Patrick Senatus, MD, PhD and Allen Waziri, MD.

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Low-grade fibrillary astrocytoma and low cellularity with minimal nuclear atypia.
Fibrillary astrocytoma with microcyst formation.
Gemistocytic astrocytoma tumor cells have eosinophilic cytoplasm with nuclei displaced to the periphery.
Characteristic pilocytic astrocytoma, long bipolar tumor cells, and Rosenthal fibers.
Anaplastic astrocytoma with high cellularity with marked nuclear atypia.
Gross specimen of a low-grade astrocytoma.
Axial CT scan, precontrast and postcontrast, shows a low-grade astrocytoma of the left frontal lobe. The tumor is nonenhancing.
Coronal postcontrast T1-weighted MRI shows a low-grade astrocytoma in the right inferior frontal lobe just above the sylvian fissure. No enhancement is present post–gadolinium administration.
Axial T2-weighted MRI shows a low-grade astrocytoma of the inferior frontal lobe with mild mass effect and no surrounding edema.
 
 
 
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