BRAIN TUMOURS

Primary intracranial tumours account for 10% of all neoplasms, and in the UK
about half of all intracranial tumours are metastatic. Primary intracranial
tumours are derived from the skull itself, or from any of the structures lying
within it, or from their tissue precursors. They may be malignant on histological
investigation but rarely metastasize outside the brain. The most common
intracranial tumours occurring in adults . Pituitary
tumours are discussed separately.

Clinical features
The clinical features of a cerebral tumour are the result of the following:
– Progressive focal neurological deficit
– Raised intracranial pressure
– Focal or generalized epilepsy.
Neurological deficit is the result of a mass effect of the tumour and surrounding
cerebral oedema. The deficit depends on the site of the tumour, e.g. a frontal
lobe tumour will initially cause personality change, apathy and
intellectual deterioration. Subsequent involvement of the frontal speech area
and motor cortex produces expressive aphasia and hemiparesis. Rapidly
growing tumours destroy cerebral tissue and loss of function is an early
feature.

Raised intracranial pressure produces headache, vomiting and papilloedema.

The headache typically changes with posture and is made worse by coughing,
sneezing, bending and straining.
As the tumour grows there is downward displacement of the brain and pressure
on the brainstem, causing drowsiness, which progresses eventually to
respiratory depression, bradycardia, coma and death. Distortion of normal
structures at a distance from the growing tumour leads to focal neurological
signs (false localizing signs). The most common are a third and sixth cranial
nerve palsy  resulting from stretching of the nerves by downward
displacement of the temporal lobes. Epilepsy Fits may be generalized or partial
in nature. The site of origin
of a partial seizure is frequently of value in localization.

Differential diagnosis
The main differential is from other intracranial mass lesions (cerebral abscess,
tuberculoma, subdural haematoma and intracranial haematoma) and a stroke,
which may have an identical clinical presentation. Benign (idiopathic)
intracranial hypertension presents with headache and papilloedema in young
obese females. Neuroimaging is normal but at lumbar puncture there is raised
CSF pressure.

Investigations
CT and MRI are useful in detecting brain tumours. MRI is of particular value in
investigation of tumours of the posterior fossa and brainstem. MR angiography
is sometimes necessary to define the site or blood supply of a mass, particularly
if surgery is planned. Positron emission tomography (PET) is sometimes helpful
to locate an occult primary tumour with metastasis. Plain skull X-rays have no
value in brain tumour
diagnosis.
– Other investigations. These include routine tests, e.g. chest X-ray if metastatic
disease is suspected. Lumbar puncture and examination of the CSF is
contraindicated with the possibility of an intracranial mass
lesion because of danger of immediate herniation of the cerebellar tonsils,
impaction within the foramen magnum and compression of the brainstem
(‘coning’).

Management
– Surgery. Surgical exploration, and either biopsy or removal of the mass, is
usually carried out to ascertain its nature. Some benign tumours, e.g.
meningiomas, can be removed in their entirety without unacceptable
damage to surrounding structures.
– Radiotherapy is given for gliomas and radiosensitive metastases and
improves survival slightly.
– Medical treatment. Cerebral oedema surrounding a tumour is rapidly reduced
by corticosteroids; i.v. or oral dexamethasone. Epilepsy is treated with anti-
convulsants. Chemotherapy has little real value in the majority
of primary or secondary brain tumours. The prognosis is very poor in patients
with malignant tumours, with only 50% survival at 2 years for high-grade
gliomas.