Disorders that can mimic brain tumours, along with diagnostic clues
| Mimic | Helpful clinical flags | Helpful investigations |
|---|---|---|
| Infection | Fever, meningism, risk factors including HIV and chemotherapy | LP (postimaging, if safe), serological testing/culture, MRI (restricted diffusion in centre of abscess), biopsy may be necessary |
| Ischaemic stroke | Hyperacute onset of neurological deficits, vascular risk factors or mechanism | CT angiography (occluded vessel), MRI (restricted diffusion in a vascular territory) |
| Haemorrhagic stroke | Hyperacute onset of neurological deficits | Serial plain CT, gradient echo or susceptibility-weighted MRI, but delayed imaging to rule out underlying tumour may be necessary |
| Demyelination including tumefactive MS | History of resolving neurological deficits, specific associated clinical features for example, optic neuritis or atrophy, internuclear ophthalmoplegia | Distribution of MRI lesions, enhancement pattern, CSF oligoclonal bands |
| Radionecrosis/pseudoprogression | Timing in relation to radiotherapy, lack of clinical deterioration | Biopsy: Lack of glial tumour markers for example, IDH-1 or vascular fibrosis/thrombosis. Imaging: Various criteria emerging |
| Autoimmune Encephalitis | Typical clinical evolution for example, NMDA-receptor encephalitis, acute time-course, resistant seizures | Inflammatory CSF without atypical cells, serology |
| Other inflammatory disorders | Typical systemic features for example, systemic lupus erythematosus, Sjögren's syndrome, sarcoidosis | Specific autoantibodies, non-caeseating granulomas in sarcoidosis |
| Lymphoma | Rapid radiological resolution with corticosteroids |
CSF, cerebrospinal fluid; CT; computerised tomography; IDH-1, isocitrate dehydrogenase; MRI, magnetic resonance imaging; MS, multiple sclerosis; NMDA, N-methyl D-aspartate.