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Neurologic Manifestations of Glioblastoma Multiforme Follow-up

  • Author: ABM Salah Uddin, MD; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
Updated: Nov 09, 2015

Further Outpatient Care

After the initial successful therapy, observe the patient regularly as an outpatient with neurologic examination and repeat MRI scans every 2 months with the chemotherapy cycles; continue every few months to follow tumor recurrence.


Further Inpatient Care

After the initial definitive treatment (surgical debulking) of glioblastoma multiforme (GBM), the patient may need further inpatient care during the ongoing radiation therapy. Chemotherapy usually is performed on an outpatient basis. Continuing outpatient follow-up care is necessary if the patient develops neurological deterioration such as acute motor weakness or depression of consciousness from the effects of therapy, increased intracranial pressure from vasogenic edema, or acute hydrocephalus from ventricular obstruction. Appropriate intervention depends on the nature of the problem (eg, steroid therapy for edema, shunting for hydrocephalus).


Inpatient & Outpatient Medications

No specific medications are recommended for GBM. However, as mentioned previously, patients may need symptomatic therapy with steroids or anticonvulsants.



Transfer requirements depend on the tumor location and its response to treatment. If the tumor is in a noneloquent area and no neurological deficit is present after treatment, the patient remains fully ambulatory. However, other patients may require assistance, such as a 3-pronged cane or a wheelchair, depending on the residual neurological deficit.



During continuing follow-up care, monitor the patient closely and treat appropriately any complications that may develop. These may be caused by ongoing treatment, such as radiation necrosis and chemotherapy-induced neuropathy, or by progression of the disease, such as recurrence or leptomeningeal spread.



With optimal treatment, the median survival of patients with glioblastoma is about 12 months. However, only 3-5% of patients survive for more than 3 years. The overall prognosis for GBM has changed little since the 1980s, despite major improvements in neuroimaging, neurosurgery, radiotherapy, and chemotherapy techniques.[18] Although histologic grading remains the most important prognostic factor, other important prognostic factors include age at diagnosis and Karnofsky performance status (KPS). Consider the following:

  • Various studies demonstrated that patients with GBM who are younger than 40 years have an 18-month survival rate of 50%, while those aged 40-60 years have an 18-month survival rate of 20% and those older than 60 years have a rate of only 10%. In some series, age appears to be an even more important prognostic factor than histology.
  • The survival of patients with GBM decreases as KPS decreases. Patients with a KPS of more than 70 have an 18-month survival rate of 34%, while those with a KPS of less than 70 have an 18-month survival rate of 13%.
  • Additional factors such as extent of surgical resection, seizures as the initial presentation, and tumor location with superficial tumors have been variably associated with outcome.
  • A recent animal study in rats investigated the use of monoclonal antibodies 8H9 as interstitial infusion showed significant volumetric response and prolonged survival (54 d for untreated rats vs 120 d for treated rats) as a potential target therapy for high-grade gliomas. [19]
  • A study by Wang et al demonstrated that overexpression of EphA7 was predictive of adverse outcomes in patients with primary and recurrent glioblastoma multiforme, independent of microvascular density (MVD) expression. Moreover, high density of both MVD and EphA7 expression predicted the disease outcome more accurately than EphA7 alone. [20]
  • A study by Liang et al demonstrated that nuclear FABP7 was preferentially expressed in infiltrative gliomas only and associated with poor prognosis in EGFR-overexpressing glioblastoma. The study suggested that FABP7 immunoreactivity could be used to monitor the EGFR-overexpressed GBM progression. [21]

Studies are focusing attention on identifying molecular markers similar to anaplastic oligodendroglioma to predict response or resistance to specific treatments. One such interest is the expression of MGMT (O6 -methylguanine–DNA methyltransferase) gene. The protein product of this gene, 06 alkyl guanine DNA-alkyl-transferase (AGAT), is shown to be a major mechanism for tumor resistance to alkylating agents. Recent clinical trials for malignant gliomas now often include determination of MGMT expression status. Several other molecular markers, such as epidermal growth factor receptor, platelet-derived growth factor receptor, vascular endothelial growth factor receptor, loss of chromosome 10, mutation or loss of the p53 gene, expression of the YKL-40 gene, loss or mutation of PTEN gene, are being investigated.

Studies are also focusing on new targets such as receptor blockade. Glutamatergic system alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor-blocker talampanel, may be beneficial in this disease. In a recent study, talampanel was added to the standard radiation and temozolomide in adults with newly diagnosed glioblastoma to estimate the overall survival as well as talampanel toxicity as a secondary measure. The study concluded that talampanel was well tolerated and compared with European Organization for Research and Treatment of Cancer (EORTC) data, median survival seemed superior (20.3 vs 14.6 mo, respectively). Therefore, talampanel can be added to radiation therapy and temozolomide without significant additional toxicity.


Patient Education

During the course of diagnosis, treatment, and follow-up care, educate the patient and family about the course and prognosis of the tumor to help them cope with the physical and emotional burden. Set this goal during discussion with the patient in the presence of family members, nurses, physicians, social services, and spiritual services. In addition, frequent contacts, regular follow-up care, and involvement of support groups are necessary.

For patient education resources, see the Cancer Center and Brain Cancer.

Contributor Information and Disclosures

ABM Salah Uddin, MD Private Practice, Norwood Neurology; Consulting Staff, Department of Neurology, St Vincent's Hospital

ABM Salah Uddin, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Medical Association

Disclosure: Nothing to disclose.


Tambi Jarmi, MD Resident Physician, Department of Internal Medicine, Carraway Methodist Medical Center

Tambi Jarmi, MD is a member of the following medical societies: American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jorge C Kattah, MD Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria

Jorge C Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Subramanian Hariharan, MD, to the development and writing of this article.

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T1-weighted axial gadolinium-enhanced MRI demonstrates an enhancing tumor of the right frontal lobe. Image courtesy of George Jallo, MD.
T2-weighted image demonstrates notable edema and midline shift. This finding is consistent with a high grade or malignant tumor. Image courtesy of George Jallo, MD.
Histopathologic slide demonstrating a glioblastoma multiforme.
Magnetic resonance spectroscopy is representative of a glioblastoma multiforme.
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