There is no single radiologic pattern of PCNSL that is pathognomonic, but several distinctive neuroimaging features can strongly suggest the diagnosis. CT scans show iso or hyperdense lesions that homogeneously enhance in 90% of cases.18 The neuroimaging technique of choice is MRI, which demonstrates an intense signal on nonenhanced T1 imaging and dense, diffuse enhancement in 90% of cases after administration of gadolinium contrast (Figure 58.1). The lesions usually have indistinct borders and less associated cerebral edema than primary gliomas or metastatic tumors.1 They may be multiple in 30-35% of cases, are frequently periventricular in location and usually involve corpus callosum, thalamus, or basal ganglia. Experience with positron emission tomography (PET) in immuno-competent patients with PCNSL is progressively growing, but does not appear to distinguish PCNSL from other malignant brain tumors.19 The use of PET in predicting response to therapy has not yet been addressed in PCNSL.

The best method to diagnose PCNSL is stereotactic biopsy of an enhancing mass lesion. Subtotal resection is not necessary therapeutically and is usual only performed when the diagnosis of lymphoma is in doubt. In some cases, the diagnosis is established by examination of a vitrectomy specimen from the eye or cytopathology or flow cytometry of cerebrospinal fluid (CSF), obviating the need for a brain biopsy. One distinctive feature of PCNSL is that corticosteroids given to relieve high intracranial pressure can have a potent acute antitumor effect that removes all CT or MRI signs of the lesions, sometimes prior to histologic diagnosis.18 However, without further treatment patients whose tumors have regressed will inevitably relapse. Therefore, whenever possible, steroids should be withheld until a diagnostic biopsy has been obtained.

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