General aspects intracranial tumours
C. B. T. ADAMS
CLASSIFICATION
Intracranial tumours constitute a major component of a neurosurgeon's work. These can be conveniently classified into three groups: (a) extracerebral; (b) intracerebral; (c) other space-occupying lesions, and these groups are expanded in Table 1 595.
PRESENTING FEATURES
Intracranial tumours, in common with other intracranial pathologies, present with signs and symptoms of raised intracranial pressure, focal neurological features, and meningeal irritation, either singly or in combination. These are:
1.Headache due to raised intracranial pressure is often labelled migraine, or ‘acute migraine’.
2.Focal neurological features which may be missed include visual field defects or truncal ataxia due to a vermis tumour of the cerebellum.
3.Meningeal irritation is the rarest presentation, but may follow a bleeding episode. This is typically from a pituitary tumour or metastatic malignant melanoma. Meningeal irritation may also be due to infiltration of the subarachnoid space by metastatic cancer or malignant glioma.
4.Other specific presentations include primary cancer elsewhere (lung or breast), a lump in the skull or orbit due to an underlying meningioma, or an endocrine disorder caused by a pituitary or third ventricular tumour.
MANAGEMENT OF INTRACRANIAL TUMOURS
Knowledge of the natural history of the tumour, its rate of growth, and the effect on the patient of doing nothing, as well as the likely risks of tumour removal, must be assessed. Other methods of treatment, such as radiotherapy, must also be considered. Patients need to be ‘managed’ rather than subjected to a single operation. An operation should not be undertaken simply because it is feasible; however, it is important not to miss a ‘window of opportunity’, such as removing a small acoustic neuroma while hearing is still intact.
The surgeon needs to manage the intracranial pressure, the effects of the tumour, the vascularity of the tumour, and the tumour itself. Intracranial pressure can be reduced by administration of steroids, if there is considerable surrounding oedema, or by shunting if hydrocephalus is present. Surgery performed on the tumour itself can only be undertaken safely if the pressure is normal; nothing is less conducive to a good result than a swollen brain herniating through a craniotomy. Anticonvulsant therapy is started 1 or 2 days prior to surgery to ensure maintenance of adequate blood levels of the drug. In the United Kingdom any patient undergoing a craniotomy for a supratentorial tumour cannot drive for a period of 1 year, even if they are free of epilepsy. Patients must be warned of this prior to surgery. Consideration should also be given to reducing the vascularity of the tumour, especially of large meningiomas (fed by the external carotid artery via the middle meningeal artery), by preoperative embolization.
The plan for a (stereotactic) biopsy, or for partial or complete tumour removal may need to be altered during surgery. The most difficult decision a surgeon has to make is ‘when to stop’. Large meningiomas, especially those affecting the skull base, are often best removed in stages rather than all at one session. The natural inclination is perhaps to continue in the hope of achieving total tumour removal. However, if part of the tumour cannot be removed, to continue and risk serious neurological damage is obviously unwise.