Glioma & Glioblastoma Treatment Malaysia

Expert glioma and glioblastoma surgery in Malaysia by Dr Nor Faizal Ahmad Bahuri — Oxford-trained neurosurgeon at KPJ Tawakkal KL. Treatment for low-grade glioma, high-grade glioma (GBM), astrocytoma and IDH-mutant gliomas.

· Updated 26 April 2026

Glioma & Glioblastoma: Treatment in Malaysia

Gliomas are the most complex tumours I treat. Unlike meningiomas, which sit on the brain surface and can often be completely excised, gliomas grow within brain tissue — infiltrating along white matter tracts, respecting no anatomical boundary, making the surgeon’s task fundamentally different.

Understanding glioma requires understanding that this is not one disease. The 2021 WHO classification identifies over 20 distinct glioma entities based on molecular markers. Two patients with what used to be called “glioblastoma” may have entirely different tumour biology, prognosis, and response to treatment.


What Is a Glioma?

Gliomas arise from glial cells — the support cells of the central nervous system. They are graded by the WHO on a scale of 1–4 based on cellular atypia, mitotic activity, and molecular characteristics:

GradeNameKey Feature
Grade 1Pilocytic AstrocytomaPrimarily paediatric; often curable with surgery
Grade 2Diffuse Astrocytoma / OligodendrogliomaSlow-growing; IDH-mutant status is favourable
Grade 3Anaplastic Astrocytoma / Anaplastic OligodendrogliomaMore aggressive; surgery + radiotherapy + chemotherapy
Grade 4Glioblastoma (GBM)Most aggressive; median survival 15–18 months with maximal treatment

Molecular Markers: Why They Matter

IDH Mutation (Isocitrate Dehydrogenase) The single most important prognostic marker in glioma. IDH-mutant gliomas (Grades 2–3) behave more favourably — patients are younger, tumours grow slower, and survival is significantly better. IDH-wildtype at Grade 2/3 behaves much like GBM and warrants aggressive treatment.

MGMT Promoter Methylation Predicts response to temozolomide chemotherapy in GBM. Methylated MGMT = better response to chemotherapy, improved survival. This test should be done on every GBM specimen.

1p/19q Codeletion Defines oligodendroglioma. Highly chemosensitive. Significantly better prognosis than astrocytoma.

TERT Promoter Mutation, EGFR Amplification Markers associated with GBM biology and treatment resistance.

I request full molecular profiling on every glioma case at the time of surgery. Treatment decisions made without molecular data in 2026 are incomplete.


Glioblastoma (GBM): What You Need to Know

GBM is the most common and aggressive primary brain tumour in adults. It is Grade 4, IDH-wildtype, and infiltrative by nature — which means complete surgical removal is not achievable. The goal of surgery is maximal safe resection: remove as much tumour as possible while preserving function.

Why does extent of resection matter if you can’t remove it all? Multiple studies confirm that patients with >98% resection survive significantly longer than those with subtotal resection, even though microscopic disease always remains. Reducing tumour bulk:

  • Relieves mass effect and oedema
  • Reduces corticosteroid dependence
  • Improves response to subsequent radiation and chemotherapy
  • Extends the time to clinical deterioration

The Stupp Protocol — the current standard of care post-surgery:

  1. Concurrent radiotherapy (60 Gy over 6 weeks) + daily temozolomide chemotherapy
  2. Adjuvant temozolomide for 6 cycles
  3. Consider tumour treating fields (TTF) device for eligible patients

With maximal treatment, median overall survival for GBM is 15–18 months. With MGMT methylation, this improves to 20–24 months. Long-term survivors (>5 years) exist and are more common with IDH-mutant disease.

I do not tell patients these numbers to discourage them. I tell them because making decisions about treatment intensity, quality of life, and time with family requires honest information.


Surgery for Glioma

Awake Craniotomy

For gliomas near eloquent cortex — speech, language, motor function — I offer awake craniotomy. The patient remains awake during the critical resection phase. I map the functional boundary in real time using direct cortical stimulation, allowing me to remove tumour up to — but not beyond — the point where neurological function is threatened.

This technique allows a significantly greater extent of resection in eloquent-region tumours compared to resection under general anaesthesia alone. The evidence is clear: patients who undergo awake craniotomy have better neurological outcomes and greater tumour removal.

5-ALA Fluorescence-Guided Surgery

5-aminolevulinic acid (5-ALA) is taken orally the night before surgery. High-grade glioma cells preferentially accumulate its metabolite, which fluoresces pink under a specific light wavelength. Under the surgical microscope, I can visualise tumour cells that appear normal white matter under standard illumination — allowing more complete resection of enhancing tumour.

Intraoperative Neuromonitoring

Motor evoked potentials (MEP) and somatosensory evoked potentials (SSEP) are monitored continuously throughout surgery. Any deterioration triggers immediate surgical pause and reassessment. This is my early warning system.

Stereotactic Biopsy

For tumours in eloquent or deep locations where open resection is too risky — or for elderly patients where tissue diagnosis is needed to guide treatment — stereotactic needle biopsy provides histopathology with minimal surgical trauma.


Low-Grade Glioma: A Different Conversation

Grade 2 gliomas (diffuse astrocytoma, oligodendroglioma) present a different challenge. They grow slowly, often present with seizures, and may not cause significant deficits for years. The temptation — especially in a young patient with a small tumour causing minimal symptoms — is to defer treatment.

The evidence does not support indefinite deferral. Early surgery for low-grade glioma:

  • Provides accurate molecular diagnosis
  • Reduces seizure burden
  • Delays malignant transformation
  • May improve long-term survival

This is not a straightforward decision and must be individualised. Age, tumour size, location, molecular profile, and patient preference all factor in. I will spend the time needed to help you understand your specific situation.


Recovery & Follow-Up

After surgery: Hospital stay 3–7 days. Neurocognitive and functional assessment. Early rehabilitation where indicated.

Post-operative MRI: Within 24–48 hours to assess extent of resection before oedema develops. This is the benchmark scan.

Oncology handover: I will personally introduce you to the neuro-oncology team at KPJ Tawakkal to begin adjuvant treatment planning without delay.

Follow-up imaging: MRI every 2–3 months for GBM. Every 6 months for stable low-grade glioma.

Pseudoprogression: An important phenomenon — the MRI may appear to worsen 1–3 months after chemoradiation, mimicking tumour growth. This is usually treatment-related inflammation, not true progression. Experience and clinical context are essential to distinguish the two.


Book a Consultation

If you or a family member has been diagnosed with a glioma — or has symptoms that raise concern — contact the clinic to arrange a consultation and MRI review.

WhatsApp the clinic: +6011 3723 5061 Book online: KPJ Tawakkal Appointment Portal Call the clinic: +603-4026 7777 ext 5099


Educational purposes only. Treatment decisions require direct consultation with a qualified neurosurgeon following review of your specific imaging and molecular data.