Brain Tumours in Adults
Brain tumours in adults include primary brain tumours, such as meningiomas, gliomas and glioblastoma, and secondary brain tumours, also known as brain metastases.
This updated UKMLA guide to brain tumours in adults is based primarily on NICE NG99, which covers primary vs secondary tumours, causes, risk factors, symptoms, diagnosis, and management.
Disclaimer:
Brain tumours are a highly specialist topic. This article provides a simplified, exam-focused overview and intentionally omits many specialist details, including detailed molecular classification and tumour-specific treatment protocols. NICE guidance contains detailed neuro-oncology recommendations; therefore, this article focuses on key shared clinical features, general investigation and management principles, and selected additional information on the most common tumour types relevant to medical students and junior doctors.
Overview and Types
In adults, the most common type of brain tumour is secondary brain tumours (brain metastasis) [Ref]
Most common types of primary brain tumours: [Ref]
- Meningiomas are the most common primary brain tumour overall (~35% of all primary brain tumours)
- Meningiomas are mostly benign and low-grade
- Gliomas are the most common malignant brain tumour
- Glioblastoma is the most common and aggressive type (~15% of all primary brain tumours and 45% of all malignant primary brain tumours)
Classifying Types of Brain Tumour
This section provides a simplified overview to aid understanding and does not cover the full classification of brain tumours.
Brain tumours are commonly described using two main questions:
- How aggressive is it? (using grade 1-4)
- What cell / tissue does it arise from? (using tumour type)
Grading and tissue of origin are related, but are independent classification systems.
1. Tumour grading:
- Grade 1-2 = low grade = slower growing and less aggressive
- Grade 3-4 = high grade = faster growing and more aggressive
Important: low-grade does not mean harmless, as even slow-growing brain tumours can cause serious symptoms due to mass effect, raised ICP or compression of important structures.
2. Cell / tissue of origin:
- Gliomas (tumours arising from glial / supporting cells of the CNS) – umbrella term covering:
- Astrocytoma
- Oligodendroglioma
- Ependymoma
- Glioblastoma (an aggressive grade 4 astrocytic glioma)
- Non-gliomas
- Meningioma
- Pituitary tumour (see the Pituitary Tumours article for more information)
- Vestibular schwannoma
- Medulloblastoma (mainly in children)
Primary Brain Tumour
Causes and Risk Factors
Exposure to ionising radiation (e.g. CT head, radiation therapy) is the only identified environmental factor
- Follows a dose-response relationship
- Most commonly results in meningiomas
There is NO increased risk of developing brain tumours from mobile phone use.
- Advancing age
- Mean age of diagnosis for meningioma = 65 y/o
- Mean age of diagnosis for glioblastoma = 64 y/o
- Family history
- Cancer predisposition syndromes
- Li Fraumeni syndrome
- Neurofibromatosis type 1
- Lynch syndrome, Cowden syndrome
- Von Hippel-Lindau-Syndrome
Clinical Features
Low-grade brain tumours (e.g. meningiomas) often present with progressive or subacute neurological symptoms. The classic triad of:
- New-onset unprovoked seizures (most common initial presentation seen in 58% of low-grade gliomas)
- Focal neurological deficits and cognitive decline
- Headache – less common in low-grade tumours
- Classic ‘brain tumour headache’: mild at onset, starts upon waking, disappears shortly after arising (but only present in 25-33% of patients)
Up to 10% of cases are asymptomatic and discovered incidentally during brain imaging for unrelated reasons
Focal neurological deficit patterns depend on the location of the tumour. High yield summary:
| Tumour location | Symptom pattern |
|---|---|
| Frontal lobe |
|
| Temporal lobe |
|
| Parietal lobe |
|
| Occipital lobe |
|
| Cerebellum |
|
High-grade tumours (e.g. glioblastoma) often present acutely where symptoms develop rapidly (over hours to weeks):
- Headache – significantly more common in high-grade tumours than low-grade tumours
- Focal neurological deficits (due to aggressive brain infiltration or oedema)
- Motor weakness (seen in ~20% patients)
- Aphasia / language difficulties (seen in ~20% patients)
- Visual disturbances
- Cognitive and behavioural decline
- Seizures – less common as an initial presenting symptom compared to low-grade tumours
High-grade brain tumours can cause intra-tumoural haemorrhage
Investigation and Diagnosis
Initial work up: neuroimaging
- 1st line: MRI brain
- If MRI is contraindicated → CT head
- Further imaging
- Consider advanced MRI techniques (e.g. MR perfusion, MR spectroscopy) for low-grade tumours on standard MRI to assess the potential of a high-grade transformation
- Consider CT imaging if bone involvement is suspected with a meningioma
Neuroimaging findings: [Ref1][Ref2]
| General brain tumour features |
|
| Meningioma features |
|
| Glioblastoma features |
|
Tissue biopsy is NOT always required, and depends on multiple factors:
- If the disease is resectable → proceed straight to resection
- If the disease is non-resectable → consider biopsy for histological and molecular diagnosis
- If imaging shows a very low-grade tumour → consider active monitoring without a histological diagnosis
Specialist testing (simplified):
Brain tumour classification is now increasingly based on molecular testing as well as histology. Molecular markers allow classification of gliomas, prognosis prediction and guide treatment.
Some examples of recommended molecular testing for gliomas:
- IDH mutation – presence is associated with a better prognosis
- 1p/19q codeletion – supports diagnosis of oligodendroglioma
- MGMT promoter methylation – informs prognosis and guides treatment decisions
Management
Management is individualised and planned by a specialist neuro-oncology MDT. The exact approach depends on tumour type, grade, location, resectability, symptoms, patient fitness and patient preference.
| Primary brain tumour | Key management approach |
|---|---|
| Meningioma | Initial approach: [Ref]
If surgery is performed, post-resection management depends on the grade and extent of surgical excision:
If surgery was not possible or declined, consider either active monitoring or radiotherapy across all grades Chemotherapy plays very little role in the management of meningiomas. |
| Low-grade gliomas | Initial approach:
If surgery is performed, post-resection management depends on a risk assessment:
|
| Glioblastoma | Initial approach:
If surgery is performed, post-resection management depends mainly on the patient’s age and the patient’s performance status / overall health (measured using the Karnofsky performance status):
|
Key management principles for acute complications: [Ref1][Ref2]
- ↑ ICP → dexamethasone
- Acute seizure → manage as Status Epilepticus if necessary
- Common practice: non-liver enzyme-inducing antiepileptic drug (avoid phenytoin, carbamazepine) due to risk of interacting with necessary medications like chemotherapy
- Primary seizure prophylaxis is NOT recommended
- Hydrocephalus → VP shunt
Patients with brain tumours (esp. gliomas) have a very high risk of developing VTE [Ref]
- Routine long-term prophylaxis is NOT recommended
- VTE prophylaxis (e.g. LMWH with mechanical methods) should be started peri-operatively
- If VTE do develop → treat with LMWH
Secondary Brain Tumours (Brain Metastases)
Secondary brain tumours occur from systemic cancer spreading to the brain parenchyma.
Causes
Common primary cancers that metastasise to the brain: [Ref]
- Lung cancer and breast cancer – most common
- Melanoma (most likely malignant to present with synchronous brain metastases)
- Kidney cancer
Clinical Features
Clinical presentation is basically the same as primary brain tumours. The classic triad of:
- Headache
- Classic ‘brain tumour headache’: mild at onset, starts upon waking, disappears shortly after arising (but only present in 25-33% of patients)
- New-onset unprovoked seizures
- Focal neurological symptoms
Also, cognitive or behavioural impairment depending on the location of the tumour (see the primary tumour clinical features section above for more details)
If the cancer has spread to the cerebrospinal fluid and the inner membranes of the brain and spinal cord (Leptomeningeal metastases), it typically presents with obstructive hydrocephalus and ↑ ICP.
Investigation and Diagnosis
Initial test: MRI brain
- Brain metastases classically appear as multiple, well-circumscribed contrast-enhancing lesions, often at the grey-white matter junction
- A solitary brain metastasis can occur, so a single lesion does not exclude metastatic disease
- They may show ring enhancement, especially if there is central necrosis
Staging is necessary with extra-cranial imaging to assess for the primary cancer (including whether it’s controlled or progressing)
Management
Treatment decisions are highly personalised and take into account the primary tumour site and molecular profile, whether the extracranial disease is controlled, the number and volume of the brain metastases, and the patient’s performance status.
| Single brain metastasis | Consider maximal local therapy:
If treated with ANY of the above, do NOT offer adjuvant whole-brain radiotherapy. |
| Multiple brain metastases | For those with good performance status and extracranial disease is controlled:
Whole-brain radiotherapy can be considered, but requires a careful discussion with the patient regarding potential benefits (tumour stabilisation) versus harms (short-term quality of life deterioration, temporary hair loss, and the potential for accelerated cognitive loss) |
Key management principles for acute complications: [Ref1][Ref2]
- ↑ ICP → dexamethasone
- Acute seizure → manage as Status Epilepticus if necessary
- Common practice: non-liver enzyme-inducing antiepileptic drug (avoid phenytoin, carbamazepine) due to risk of interacting with necessary medications like chemotherapy
- Primary seizure prophylaxis is NOT recommended
- Hydrocephalus → VP shunt