Common brain tumours

Common brain tumours

Cerebral metastases Cerebral metastases ( Figure 48.21 ) are the most common intracranial tumours and are diagnosed in 25% of patients with cancer, a proportion that is increasing with extended survival associated with more e ff ective treatment of primary cancers. The tumours of origin and their contribution to the burden of cerebral metastases are detailed in Table 48.7 . Traditionally Robert Foster Kennedy , 1884–1952, British Neurologist, awarded the Chevalier de la Légion d’honneur in recognition of his service in French front-line field hospitals in the First World War. Josef Gerstmann , 1887–1969, Austrian neurologist who fled to America in 1938 to escape the Nazis. - ).

certain tumours. Tumour location Expected de /f_i cit Pituitary (e.g. pituitary Bitemporal hemianopia; gaze adenoma) palsies Cerebellopontine angle (e.g. Hearing loss; balance vestibular schwannoma) disturbance; tinnitus Anterior skull base (e.g. Anosmia; ipsilateral optic olfactory groove meningioma) atrophy; contralateral papilloedema (Foster Kennedy syndrome) Occipital (e.g. glioma, Homonymous hemianopia with metastasis) central sparing Parietal (dominant hemisphere) Acalculia; agraphia; left–right disorientation; /f_i nger agnosia (Gerstmann’s syndrome) Parietal (e.g. glioma) Sensory inattention; dressing apraxia; astereognosis Temporal (e.g. glioma) Memory disturbance; contralateral superior quadrantanopia; dysphasia (dominant hemisphere) Frontal (e.g. glioma) Personality change; gait disturbance; urinary incontinence Brainstem (e.g. brainstem Multiple cranial nerve de /f_i cits; glioma) long tract signs; nystagmus Posterior fossa (e.g. Ataxia; hydrocephalus medulloblastoma) Figure 48.21 T1-weighted magnetic resonance imaging with contrast. Two right occipital lung metastases are demonstrated. They are well demarcated and enhance with gadolinium contrast.

able for surgery . In patients with good functional status and well-controlled systemic disease, craniotomy for resection of a single focus, and in selected cases multiple lesions, may confer symptomatic and survival benefits. New molecular therapies can control systemic disease in man y cancers; in these cases craniotomy and resection of one or more lesions responsible for the mass e ff ect or hydrocephalus with medical treatment of the remaining lesions may be well warranted. Occasionally diagnostic biopsy may be warranted where the primary is unknown. Glioma These are intrinsic tumours with glial histology , with subtypes including astrocytomas, oligodendrogliomas, ependymomas and mixed tumours. This is a tissue diagnosis, but imaging often predicts both a glial origin and the grade of tumour ( Figure 48.22 ). Low-grade glioma (WHO grade II) has a peak incidence in the fourth decade of life, and commonly presents with seizures initially . High-grade gliomas include anaplastic astrocytoma (WHO grade III) and glioblastoma (WHO grade IV), the commonest glial tumour ( Figure 48.23 de novo with the peak incidence in the fifth and typically present sixth decades of life, respectively , or arise by transformation of low-grade tumours. MRI of the head with and without contrast is the preferred modality , generally combined with CT of the chest, abdomen and pelvis to exclude an extracranial primary , since metastasis is usually the main di ff erential diagnosis. Di ff usion-weighted MRI sequences are valuable in excluding another key di ff er - ential diagnosis – brain abscess , which is associated with prom - inent restricted di ff usion in these images. Initial management of these tumours should generally include high-dose steroids to alleviate any mass e ff ect. Anti- epileptics are administered when seizures are a presenting feature or are anticipated in view of the temporal loca tion. Sur - ). They gical resection is usually the primary treatment, with the aim of reducing disease burden and obtaining tissue for diagnosis. When tumours encroach on the eloquent cortex, especially the speech areas of the dominant hemisphere which are not consistently ana tomically localised, awake craniotomy allows for mapping of speech function. Except for grade I pilocytic astrocytomas typically found in children, gliomas are notable for di ff use infiltration into the surrounding brain, so that recur - rence after even macroscopically complete resection is the rule. The classification of gliomas has been significantly updated with the recent addition of integrated molecular diagnostic categories to the WHO 2016 classification ( Figure 48.24 ). Gliomas with low-grade histolog y often carry characteristic mutations; for example, point mutations in isocitrate dehydro - genase ( IDH ) enzymes and 1p/19q chromosomal co-deletion, the latter specific to oligodendrogliomas. Glioblastomas are WHO grade IV tumours and include IDH wild-type ‘primary’ glioblastoma and occasional IDH mutant ‘secondary’ glioblas - tomas. These are thought to arise from transformation of pre - viously diagnosed, or clinically silent, low-grade gliomas. IDH wild-type status is a strong predictor of aggressive malignant behaviour, even in the absence of high-grade histological fea - tures. Active treatment consists of maximal surgical resection, typically with the assistance of intraoperative neuronavigation systems to accurately localise the tumour.

TABLE 48.7 Tissue of origin for brain metastases (approximate). Origin Percentage Lung 40 Breast 15 Melanoma 10 Renal/genitourinary 10 Other/unknown 25 Figure 48.22 Computed tomography with contrast demonstrates a heterogeneous right frontoparietal lesion with mass effect and midline shift, almost certainly a glioblastoma multiforme. A magnetic reso nance imaging scan with and without contrast will aid evaluation. Figure 48.23 Pathological specimen of glioblastoma multiforme.

Patients can also be dosed with 5-aminolevulinic acid (5-ALA) preoperatively . Protoporphyrin IX, a fluorescent metabolite of this drug, accumulates selectively in glioma cells, causing them to glow pink under ultraviolet light, so providing a real-time assessment of tumour infiltration at the resection boundaries. First-line adjuvant treatment in malignant glioma includes high-dose focused radiation therapy and alkylating chemother apy with oral temozolomide. Median survival for glioblastoma remains just over 12 months. Meningioma Meningiomas are usually benign lesions, although anaplastic variants do occur. They arise from the meninges and typi cally present as a result of the mass e ff ect from the tumour, compounded by vasogenic oedema in the adjacent brain and obstructive hydrocephalus where CSF drainage is impair Imaging will demonstrate a contrast-enhancing mass distinct from the brain with a dural base ( Figure 48.25 ). These are generally slow-growing lesions: smaller lesions, perhaps detected incidentally in an elderly patient, may well warrant a ‘watch-and-wait’ approach. If the lesion is large or positioned so as to impinge on key structures, the patient may requir e steroids and early surgery . The degree of resection pre dicts recurrence, with rates of 10% at 10 years for total excision with a clear dural margin and 30% at 10 years for subtotal excision. Lesions that are di ffi cult to approach surgically may be managed with radiotherapy or stereotactic radiosurgery Martin Heinrich Rathke , 1793–1860, German anatomist. α Summary box 48.10 Common supratentorial brain tumours /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF ed.

IDH status IDH mutant 1p/19q and a ATRX loss 1p/19q other genetic a TP53 mutation co-deletion parameters Diffuse astrocytoma, IDH mutant Oligodendroglioma, IDH mutant and 1p/19q co-deleted After exclusion of other entities: Diffuse astrocytoma, Oligodendroglioma, NOS Figure 48.24 World Health Organization 2016 classi /f_i cation of gliomas. ATRX, a IDH, isocitrate dehydrogenase; NOS, not otherwise speci /f_i ed. A, Reifenberger G et al . The 2016 World Health Organization classi /f_i cation of tumors of the central nervous system: a summary. 2016; 131 (6): 803–20, with permission from Springer.) IDH wild type IDH mutant IDH wild type Glioblastoma, IDH mutant Glioblastoma, IDH wild type Genetic testing not done or inconclusive Diffuse astrocytoma, NOS Oligodendroglioma, NOS IDH wild type Oligoastrocytoma, NOS Glioblastoma, NOS -thalassaemia/mental retardation syndrome X-linked; Characteristic but not required for diagnosis. (Reproduced from Louis DN, Perry Acta Neuropathol Metastases and gliomas are common tumours arising within brain substance, appearing as ‘ring-enhancing’ lesions on contrast CT. Surgery is usually life-extending rather than curative Meningiomas arise from the meninges around the brain and typically enhance uniformly on contrast CT. Most are benign and amenable to curative resection MRI is usually the best modality for evaluating brain tumours. Diffusion-weighted sequences help to exclude abscess when glioma or metastasis is suspected Metastasis is the main differential diagnosis, and CT of the body is useful in identifying extracranial primary tumours Steroids, along with proton pump inhibitor treatment for gastric protection, are administered to control swelling and the mass effect in the short term

Common brain tumours

Cerebral metastases Cerebral metastases ( Figure 48.21 ) are the most common intracranial tumours and are diagnosed in 25% of patients with cancer, a proportion that is increasing with extended survival associated with more e ff ective treatment of primary cancers. The tumours of origin and their contribution to the burden of cerebral metastases are detailed in Table 48.7 . Traditionally Robert Foster Kennedy , 1884–1952, British Neurologist, awarded the Chevalier de la Légion d’honneur in recognition of his service in French front-line field hospitals in the First World War. Josef Gerstmann , 1887–1969, Austrian neurologist who fled to America in 1938 to escape the Nazis. - ).

certain tumours. Tumour location Expected de /f_i cit Pituitary (e.g. pituitary Bitemporal hemianopia; gaze adenoma) palsies Cerebellopontine angle (e.g. Hearing loss; balance vestibular schwannoma) disturbance; tinnitus Anterior skull base (e.g. Anosmia; ipsilateral optic olfactory groove meningioma) atrophy; contralateral papilloedema (Foster Kennedy syndrome) Occipital (e.g. glioma, Homonymous hemianopia with metastasis) central sparing Parietal (dominant hemisphere) Acalculia; agraphia; left–right disorientation; /f_i nger agnosia (Gerstmann’s syndrome) Parietal (e.g. glioma) Sensory inattention; dressing apraxia; astereognosis Temporal (e.g. glioma) Memory disturbance; contralateral superior quadrantanopia; dysphasia (dominant hemisphere) Frontal (e.g. glioma) Personality change; gait disturbance; urinary incontinence Brainstem (e.g. brainstem Multiple cranial nerve de /f_i cits; glioma) long tract signs; nystagmus Posterior fossa (e.g. Ataxia; hydrocephalus medulloblastoma) Figure 48.21 T1-weighted magnetic resonance imaging with contrast. Two right occipital lung metastases are demonstrated. They are well demarcated and enhance with gadolinium contrast.

able for surgery . In patients with good functional status and well-controlled systemic disease, craniotomy for resection of a single focus, and in selected cases multiple lesions, may confer symptomatic and survival benefits. New molecular therapies can control systemic disease in man y cancers; in these cases craniotomy and resection of one or more lesions responsible for the mass e ff ect or hydrocephalus with medical treatment of the remaining lesions may be well warranted. Occasionally diagnostic biopsy may be warranted where the primary is unknown. Glioma These are intrinsic tumours with glial histology , with subtypes including astrocytomas, oligodendrogliomas, ependymomas and mixed tumours. This is a tissue diagnosis, but imaging often predicts both a glial origin and the grade of tumour ( Figure 48.22 ). Low-grade glioma (WHO grade II) has a peak incidence in the fourth decade of life, and commonly presents with seizures initially . High-grade gliomas include anaplastic astrocytoma (WHO grade III) and glioblastoma (WHO grade IV), the commonest glial tumour ( Figure 48.23 de novo with the peak incidence in the fifth and typically present sixth decades of life, respectively , or arise by transformation of low-grade tumours. MRI of the head with and without contrast is the preferred modality , generally combined with CT of the chest, abdomen and pelvis to exclude an extracranial primary , since metastasis is usually the main di ff erential diagnosis. Di ff usion-weighted MRI sequences are valuable in excluding another key di ff er - ential diagnosis – brain abscess , which is associated with prom - inent restricted di ff usion in these images. Initial management of these tumours should generally include high-dose steroids to alleviate any mass e ff ect. Anti- epileptics are administered when seizures are a presenting feature or are anticipated in view of the temporal loca tion. Sur - ). They gical resection is usually the primary treatment, with the aim of reducing disease burden and obtaining tissue for diagnosis. When tumours encroach on the eloquent cortex, especially the speech areas of the dominant hemisphere which are not consistently ana tomically localised, awake craniotomy allows for mapping of speech function. Except for grade I pilocytic astrocytomas typically found in children, gliomas are notable for di ff use infiltration into the surrounding brain, so that recur - rence after even macroscopically complete resection is the rule. The classification of gliomas has been significantly updated with the recent addition of integrated molecular diagnostic categories to the WHO 2016 classification ( Figure 48.24 ). Gliomas with low-grade histolog y often carry characteristic mutations; for example, point mutations in isocitrate dehydro - genase ( IDH ) enzymes and 1p/19q chromosomal co-deletion, the latter specific to oligodendrogliomas. Glioblastomas are WHO grade IV tumours and include IDH wild-type ‘primary’ glioblastoma and occasional IDH mutant ‘secondary’ glioblas - tomas. These are thought to arise from transformation of pre - viously diagnosed, or clinically silent, low-grade gliomas. IDH wild-type status is a strong predictor of aggressive malignant behaviour, even in the absence of high-grade histological fea - tures. Active treatment consists of maximal surgical resection, typically with the assistance of intraoperative neuronavigation systems to accurately localise the tumour.

TABLE 48.7 Tissue of origin for brain metastases (approximate). Origin Percentage Lung 40 Breast 15 Melanoma 10 Renal/genitourinary 10 Other/unknown 25 Figure 48.22 Computed tomography with contrast demonstrates a heterogeneous right frontoparietal lesion with mass effect and midline shift, almost certainly a glioblastoma multiforme. A magnetic reso nance imaging scan with and without contrast will aid evaluation. Figure 48.23 Pathological specimen of glioblastoma multiforme.

Patients can also be dosed with 5-aminolevulinic acid (5-ALA) preoperatively . Protoporphyrin IX, a fluorescent metabolite of this drug, accumulates selectively in glioma cells, causing them to glow pink under ultraviolet light, so providing a real-time assessment of tumour infiltration at the resection boundaries. First-line adjuvant treatment in malignant glioma includes high-dose focused radiation therapy and alkylating chemother apy with oral temozolomide. Median survival for glioblastoma remains just over 12 months. Meningioma Meningiomas are usually benign lesions, although anaplastic variants do occur. They arise from the meninges and typi cally present as a result of the mass e ff ect from the tumour, compounded by vasogenic oedema in the adjacent brain and obstructive hydrocephalus where CSF drainage is impair Imaging will demonstrate a contrast-enhancing mass distinct from the brain with a dural base ( Figure 48.25 ). These are generally slow-growing lesions: smaller lesions, perhaps detected incidentally in an elderly patient, may well warrant a ‘watch-and-wait’ approach. If the lesion is large or positioned so as to impinge on key structures, the patient may requir e steroids and early surgery . The degree of resection pre dicts recurrence, with rates of 10% at 10 years for total excision with a clear dural margin and 30% at 10 years for subtotal excision. Lesions that are di ffi cult to approach surgically may be managed with radiotherapy or stereotactic radiosurgery Martin Heinrich Rathke , 1793–1860, German anatomist. α Summary box 48.10 Common supratentorial brain tumours /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF ed.

IDH status IDH mutant 1p/19q and a ATRX loss 1p/19q other genetic a TP53 mutation co-deletion parameters Diffuse astrocytoma, IDH mutant Oligodendroglioma, IDH mutant and 1p/19q co-deleted After exclusion of other entities: Diffuse astrocytoma, Oligodendroglioma, NOS Figure 48.24 World Health Organization 2016 classi /f_i cation of gliomas. ATRX, a IDH, isocitrate dehydrogenase; NOS, not otherwise speci /f_i ed. A, Reifenberger G et al . The 2016 World Health Organization classi /f_i cation of tumors of the central nervous system: a summary. 2016; 131 (6): 803–20, with permission from Springer.) IDH wild type IDH mutant IDH wild type Glioblastoma, IDH mutant Glioblastoma, IDH wild type Genetic testing not done or inconclusive Diffuse astrocytoma, NOS Oligodendroglioma, NOS IDH wild type Oligoastrocytoma, NOS Glioblastoma, NOS -thalassaemia/mental retardation syndrome X-linked; Characteristic but not required for diagnosis. (Reproduced from Louis DN, Perry Acta Neuropathol Metastases and gliomas are common tumours arising within brain substance, appearing as ‘ring-enhancing’ lesions on contrast CT. Surgery is usually life-extending rather than curative Meningiomas arise from the meninges around the brain and typically enhance uniformly on contrast CT. Most are benign and amenable to curative resection MRI is usually the best modality for evaluating brain tumours. Diffusion-weighted sequences help to exclude abscess when glioma or metastasis is suspected Metastasis is the main differential diagnosis, and CT of the body is useful in identifying extracranial primary tumours Steroids, along with proton pump inhibitor treatment for gastric protection, are administered to control swelling and the mass effect in the short term

Common brain tumours

Cerebral metastases Cerebral metastases ( Figure 48.21 ) are the most common intracranial tumours and are diagnosed in 25% of patients with cancer, a proportion that is increasing with extended survival associated with more e ff ective treatment of primary cancers. The tumours of origin and their contribution to the burden of cerebral metastases are detailed in Table 48.7 . Traditionally Robert Foster Kennedy , 1884–1952, British Neurologist, awarded the Chevalier de la Légion d’honneur in recognition of his service in French front-line field hospitals in the First World War. Josef Gerstmann , 1887–1969, Austrian neurologist who fled to America in 1938 to escape the Nazis. - ).

certain tumours. Tumour location Expected de /f_i cit Pituitary (e.g. pituitary Bitemporal hemianopia; gaze adenoma) palsies Cerebellopontine angle (e.g. Hearing loss; balance vestibular schwannoma) disturbance; tinnitus Anterior skull base (e.g. Anosmia; ipsilateral optic olfactory groove meningioma) atrophy; contralateral papilloedema (Foster Kennedy syndrome) Occipital (e.g. glioma, Homonymous hemianopia with metastasis) central sparing Parietal (dominant hemisphere) Acalculia; agraphia; left–right disorientation; /f_i nger agnosia (Gerstmann’s syndrome) Parietal (e.g. glioma) Sensory inattention; dressing apraxia; astereognosis Temporal (e.g. glioma) Memory disturbance; contralateral superior quadrantanopia; dysphasia (dominant hemisphere) Frontal (e.g. glioma) Personality change; gait disturbance; urinary incontinence Brainstem (e.g. brainstem Multiple cranial nerve de /f_i cits; glioma) long tract signs; nystagmus Posterior fossa (e.g. Ataxia; hydrocephalus medulloblastoma) Figure 48.21 T1-weighted magnetic resonance imaging with contrast. Two right occipital lung metastases are demonstrated. They are well demarcated and enhance with gadolinium contrast.

able for surgery . In patients with good functional status and well-controlled systemic disease, craniotomy for resection of a single focus, and in selected cases multiple lesions, may confer symptomatic and survival benefits. New molecular therapies can control systemic disease in man y cancers; in these cases craniotomy and resection of one or more lesions responsible for the mass e ff ect or hydrocephalus with medical treatment of the remaining lesions may be well warranted. Occasionally diagnostic biopsy may be warranted where the primary is unknown. Glioma These are intrinsic tumours with glial histology , with subtypes including astrocytomas, oligodendrogliomas, ependymomas and mixed tumours. This is a tissue diagnosis, but imaging often predicts both a glial origin and the grade of tumour ( Figure 48.22 ). Low-grade glioma (WHO grade II) has a peak incidence in the fourth decade of life, and commonly presents with seizures initially . High-grade gliomas include anaplastic astrocytoma (WHO grade III) and glioblastoma (WHO grade IV), the commonest glial tumour ( Figure 48.23 de novo with the peak incidence in the fifth and typically present sixth decades of life, respectively , or arise by transformation of low-grade tumours. MRI of the head with and without contrast is the preferred modality , generally combined with CT of the chest, abdomen and pelvis to exclude an extracranial primary , since metastasis is usually the main di ff erential diagnosis. Di ff usion-weighted MRI sequences are valuable in excluding another key di ff er - ential diagnosis – brain abscess , which is associated with prom - inent restricted di ff usion in these images. Initial management of these tumours should generally include high-dose steroids to alleviate any mass e ff ect. Anti- epileptics are administered when seizures are a presenting feature or are anticipated in view of the temporal loca tion. Sur - ). They gical resection is usually the primary treatment, with the aim of reducing disease burden and obtaining tissue for diagnosis. When tumours encroach on the eloquent cortex, especially the speech areas of the dominant hemisphere which are not consistently ana tomically localised, awake craniotomy allows for mapping of speech function. Except for grade I pilocytic astrocytomas typically found in children, gliomas are notable for di ff use infiltration into the surrounding brain, so that recur - rence after even macroscopically complete resection is the rule. The classification of gliomas has been significantly updated with the recent addition of integrated molecular diagnostic categories to the WHO 2016 classification ( Figure 48.24 ). Gliomas with low-grade histolog y often carry characteristic mutations; for example, point mutations in isocitrate dehydro - genase ( IDH ) enzymes and 1p/19q chromosomal co-deletion, the latter specific to oligodendrogliomas. Glioblastomas are WHO grade IV tumours and include IDH wild-type ‘primary’ glioblastoma and occasional IDH mutant ‘secondary’ glioblas - tomas. These are thought to arise from transformation of pre - viously diagnosed, or clinically silent, low-grade gliomas. IDH wild-type status is a strong predictor of aggressive malignant behaviour, even in the absence of high-grade histological fea - tures. Active treatment consists of maximal surgical resection, typically with the assistance of intraoperative neuronavigation systems to accurately localise the tumour.

TABLE 48.7 Tissue of origin for brain metastases (approximate). Origin Percentage Lung 40 Breast 15 Melanoma 10 Renal/genitourinary 10 Other/unknown 25 Figure 48.22 Computed tomography with contrast demonstrates a heterogeneous right frontoparietal lesion with mass effect and midline shift, almost certainly a glioblastoma multiforme. A magnetic reso nance imaging scan with and without contrast will aid evaluation. Figure 48.23 Pathological specimen of glioblastoma multiforme.

Patients can also be dosed with 5-aminolevulinic acid (5-ALA) preoperatively . Protoporphyrin IX, a fluorescent metabolite of this drug, accumulates selectively in glioma cells, causing them to glow pink under ultraviolet light, so providing a real-time assessment of tumour infiltration at the resection boundaries. First-line adjuvant treatment in malignant glioma includes high-dose focused radiation therapy and alkylating chemother apy with oral temozolomide. Median survival for glioblastoma remains just over 12 months. Meningioma Meningiomas are usually benign lesions, although anaplastic variants do occur. They arise from the meninges and typi cally present as a result of the mass e ff ect from the tumour, compounded by vasogenic oedema in the adjacent brain and obstructive hydrocephalus where CSF drainage is impair Imaging will demonstrate a contrast-enhancing mass distinct from the brain with a dural base ( Figure 48.25 ). These are generally slow-growing lesions: smaller lesions, perhaps detected incidentally in an elderly patient, may well warrant a ‘watch-and-wait’ approach. If the lesion is large or positioned so as to impinge on key structures, the patient may requir e steroids and early surgery . The degree of resection pre dicts recurrence, with rates of 10% at 10 years for total excision with a clear dural margin and 30% at 10 years for subtotal excision. Lesions that are di ffi cult to approach surgically may be managed with radiotherapy or stereotactic radiosurgery Martin Heinrich Rathke , 1793–1860, German anatomist. α Summary box 48.10 Common supratentorial brain tumours /uni25CF /uni25CF - /uni25CF /uni25CF - /uni25CF ed.

IDH status IDH mutant 1p/19q and a ATRX loss 1p/19q other genetic a TP53 mutation co-deletion parameters Diffuse astrocytoma, IDH mutant Oligodendroglioma, IDH mutant and 1p/19q co-deleted After exclusion of other entities: Diffuse astrocytoma, Oligodendroglioma, NOS Figure 48.24 World Health Organization 2016 classi /f_i cation of gliomas. ATRX, a IDH, isocitrate dehydrogenase; NOS, not otherwise speci /f_i ed. A, Reifenberger G et al . The 2016 World Health Organization classi /f_i cation of tumors of the central nervous system: a summary. 2016; 131 (6): 803–20, with permission from Springer.) IDH wild type IDH mutant IDH wild type Glioblastoma, IDH mutant Glioblastoma, IDH wild type Genetic testing not done or inconclusive Diffuse astrocytoma, NOS Oligodendroglioma, NOS IDH wild type Oligoastrocytoma, NOS Glioblastoma, NOS -thalassaemia/mental retardation syndrome X-linked; Characteristic but not required for diagnosis. (Reproduced from Louis DN, Perry Acta Neuropathol Metastases and gliomas are common tumours arising within brain substance, appearing as ‘ring-enhancing’ lesions on contrast CT. Surgery is usually life-extending rather than curative Meningiomas arise from the meninges around the brain and typically enhance uniformly on contrast CT. Most are benign and amenable to curative resection MRI is usually the best modality for evaluating brain tumours. Diffusion-weighted sequences help to exclude abscess when glioma or metastasis is suspected Metastasis is the main differential diagnosis, and CT of the body is useful in identifying extracranial primary tumours Steroids, along with proton pump inhibitor treatment for gastric protection, are administered to control swelling and the mass effect in the short term