CT scan

Contrast enhanced CT scan is usually the initial investigation in patients suspected to have a brain lesion. CT scan is not an ideal investigation for low-grade tumours or tumours in the posterior fossa. CT scan may also show features of oedema, hydrocephalus, haemorrhage and calcification depending on the histological variant of brain tumour. Table 16.1 shows radiological appearance of common tumours.

Table 16.1 Radiological appearance of common brain tumours

MRI scan

MRI scan with gadolinium and FLAIR (fluid-attenuated inversion recovery) sequence is the standard investigation for brain tumours. T1W imaging demonstrates anatomy and areas of contrast enhancement and T2W and FLAIR images are useful in demonstrating oedema. Appearance of tumour on T1W image is similar to that on CT, but better delineated on MRI. Tumour and oedema demonstrate increased signal on T2 and the area of increased T2 signal on MRI usually includes the hypodense area on CT (Figure 16.1).

Figure 16.1 MRI scan of diffuse astrocytoma. Scan shows hypointense lesion on left parieto-occipital region (A) without contrast enhancement (B) on T1W image. T2W image (C) shows a hyperintense lesion. Since low-grade tumours are not associated with oedema, this hyperintense lesion represents just the tumour.

Various MR imaging techniques are being evolved to improve the diagnostic ability in the imaging of brain tumours.

Evaluation of the craniospinal axis

MRI of the craniospinal axis and CSF evaluation is needed for tumours with a high risk of CSF dissemination such as medulloblastoma, germ cell tumours, CNS lymphoma, PNET and ependymoma (Figure 16.2). CSF evaluation includes CSF biochemistry (typically elevated protein >40 mg/dL and reduced glucose <50 mg/mL), cytology and in cases of suspected germ cell tumours, the estimation of tumour markers (AFP and beta hCG) in CSF and serum. Evaluation of the craniospinal axis is best done prior to surgery or >3 weeks after surgery to avoid false positive results.

Figure 16.2 Multiple contrast-enhancing tumour nodules in ependymoma suggesting leptomeningeal disease.

Tissue diagnosis

Histologic confirmation is necessary in all patients prior to definite treatment. Biopsy is obtained by either stereotactic guided techniques or open biopsy. In intrinsic brainstem tumours, biopsy may cause neurologic damage and hence may be avoided. Biopsy is avoided in patients with multiple brain metastases from a known primary, optic meningioma and CNS lymphoma in HIV positive patients showing typical radiological findings.

Steroids

Steroids may improve symptoms by reducing intracranial pressure. The most commonly used agent is dexamethasone which is started at a dose of 2–16 mg daily (low doses given once daily and higher doses as 2–4 equally divided doses) and titrated against the patient’s symptoms. The optimal dose is just above that at which symptomatic deterioration occurs. If there is no symptomatic improvement, steroids should be stopped.

Anti-epileptics

All patients who have had a seizure should be treated with an anti-epileptic drug (AED); prophylactic use of anti-epileptics is not recommended. Many anti-epileptics are enzyme-inducers, and hence should be carefully monitored when they need to be used concurrently with drugs metabolized by cytochrome p450 enzyme system.

Analgesics

Patients requiring pain control are managed according to the WHO analgesic ladder (p. 66).

Radiation tolerance and reactions

Radiation to the brain can cause structural damage to critical structures if attention is not paid not to exceed the tolerance dose of individual structures.

Acute radiation reactions may manifest up to 6 weeks following completion of irradiation. These reactions are generally those of raised intracranial pressure, fatigue and worsening of neurology. Vomiting is particularly common in patients receiving radiotherapy to the brainstem region.

Early delayed (intermediate) side effects usually appear from 6 weeks to 6 months following radiotherapy and are due to changes in capillary permeability and transient demyelination. Symptoms include headache, somnolence syndrome, lethargy and frequently recurrence of the original presenting features. Recovery is spontaneous but can be accelerated by steroids.

Delayed radiation reaction develops 6 months after radiotherapy. This is thought to be due to white matter injury secondary to vascular injury, demyelination and necrosis. The most serious form of this is radiation necrosis which peaks at 3 years. Conventional imaging fails to distinguish this from recurrent tumour and special imaging is therefore needed (p. 265). Treatment is with steroids and debulking. Other late effects include, depending on the area irradiated, memory problems, pituitary failure, hearing loss, visual changes and second malignancies.