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23 Cards in this Set
- Front
- Back
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better called intracranial neoplasms
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some dont arise from brain tissue
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incidence
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15/100,000/year
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Risk factors
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Irradiation of the cranium is the only unequivocal risk factor – Possible risk factors: high-tension wires, head trauma, mobile phones, parental exposure to diesel exhausts (childhood brain tumours) |
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ICP
- normal - compensation - pressures |
•ICP: the pressure of CSF in the cranial cavity
•Intracranial contents contributing to pressure –Brain tissue (75% water) –Blood –Cerebrospinal fluid •Normal range 0-15 mm Hg (above 30 mm requires treatment) •Spatial compensation initially –More effective with slowly-growing lesions •Intracranial pressure-volume relationships –At high pressures, a small increase in volume causes a large increase in pressure |
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Brain Swelling
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•Cerebral edema
–Types (often combined) •Vasogenic (breakdown of blood-brain-barrier, mostly in white matter) •Cytotoxic – grey and white matter, mostly astrocytic swelling (impairment of Na-K membrane pump, aquaporins) –Aquaporins upregulated in some brain tumours, but aquaporins have both edema forming and elimination functions •Congestive brain swelling –Vasodilation of capillaries and venules •Hypercapnia, central neurogenic |
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Consequences of intracranial expanding lesions
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• Narrowed sulci, flattened gyri
•Compression of ventricles •Herniations –Under the falx - anterior cerebral artery compression –Through the cerebellar tent •Lateral (hippocampus) - posterior cerebral artery, 3rd cranial nerve compression •Central - hemorrhages in brain stem –Cerebellar tonsils through the foramen magnum |
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Causes of raised pressure
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Tumour itself – Cerebral edema (especially vasogenic) – Tumour blocks CSF pathway (hydrocephalus) |
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Symptoms of raised intracranial pressure
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Diffuse headache • Worse in morning, and with straining, coughing • Headache can be unilateral, throbbing, like migraine – Nausea, vomiting, sixth nerve palsy, papilledema – Coma, death |
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Brain tumours Focal presentations
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•Progressive neurological deficits (loss of function)
–Symptoms reflect site of tumour (e.g. dysphasia, hemiparesis, cognitive dysfunction) –Rate of progression of symptoms reflects degree of malignancy –Usually subacute onset, except for unrecognised visual field defect •Seizures (gain of function) –Seizures first symptom in 15-95% (especially when cortical and slow growing) –Typically focal seizures |
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Brain Tumour Dx
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•CT can miss some tumours
•Cranial MRI with contrast injection –Contrast agent gets through new capillaries lacking a blood-brain-barrier –If MRI negative, essentially rules out a brain tumour •PET can help distinguish between low and high grade tumours •Diagnosis must be confirmed by histological examination –Clinical, imaging and pathological data must be in accordance (best to have multidisciplinary team discussion before treatment) |
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Common intracranial tumours
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•Glial
–Astrocytic –Oligodendroglial •Meningioma •Schwannoma •Metastatic Children have a different spectrum of tumours |
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Glial tumours are graded on
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–Abnormal nuclei (pleomorphism)
–Mitoses –Proliferation of small blood vessels –Necrosis |
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Major Prognostic factors
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–Tumour grade
–Age –Clinical status –These influence outcome more than treatment |
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Glial Tumours
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Striking propensity to infiltrate throughout the brain • Most low-grade gliomas undergo malignant transformation over the years • Biopsied samples are not necessarily representative • Separating astrocytic and oligodendroglial tumours can be difficult • Tumours with same morphology can be genetically different (and have different courses) • Appear to arise from neural stem cells or progenitor cells |
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Glioblastoma multiforme
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•The commonest malignant astrocytoma in 50-70 year-olds
•Median survival one year •Almost never metastasise outside the head •MRI: irregular ring-like contrast enhancement •Macroscopic: variegated (“multiforme”) •Microscopy: necrosis with palisading of cells, vascular proliferation •Two types (primary and secondary), based on genetic changes found |
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Treatment of GBM
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•Surgery*
•Radiotherapy* •Chemotherapy* –Temozolomide (alkylating agent, depletes the DNA repair enzyme MGMT) –Two-year post-surgical survival with radiotherapy alone: 10%, but with radiotherapy plus temozolomide: 27% –Median survival still only 15 months •Anti-angiogenesis agents –Bevacizumab (a monoclonal antibody that inhibits VEGF) –Do these agents reduce edema only? •Numerous other agents under development •Cognitive rehabilitation |
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Outcome of GBM after surgery depends on
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•Age of patient
–Younger patients do better •Extent of resection –Complete resection of the tumour appears to give a better prognosis –Randomised studies not feasible •Performance status (e.g. Karnofsky score) •Mini-mental status examination (MMSE) •Methylation status of the MGMT promoter –Longer survival time if tumour MGMT promoter is methylated (patients then have low activity of MGMT) |
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Low grade astrocytoma
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•Found in young adults
•First symptom often a seizure •Median survival 7 years •MRI: non-enhancing mass –Borders look distinct on MRI (but are not histologically) |
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Oligodendroglioma
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•20% of glial tumours
•Look like astrocytoma on imaging •Microscopy –Fried-egg appearance •Median survival –12 years with 1p/19q loss –8 years without this loss |
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Treatment of low grade gliomas
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•Surgical resection
–Particularly if progression –Tumour often too widespread •Radiation –Consider long-term side-effects •Temozolomide –Especially effective if tumour has combined 1p/19q loss of heterozygosity (? because better natural history already) –May be useful not only in oligodendroglioma, but in low grade glioma as well |
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Meningioma
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•Arise from arachnoid cells
•Majority are asymptomatic •Symptoms –Over hemispheres (seizures, progressive hemiparesis) –Skull base (cranial neuropathies) •Whorls of cells on microscopy •Slow growing •MRI –Attached to dura –Contrast enhancement (blood supply from external carotid) •Treatment: resection |
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Schwannoma
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•Common site is at the angle between the cerebellum and the pons
–Tinnitus, hearing difficulties, abnormal facial sensation •Arise from peripheral nerve Schwann cells •MRI –Well defined mass •Pathology –Spindle shaped cells with lining up of nuclei •Treatment: resection (try to preserve nerve) |
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Metastatic brain tumours
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•Common sources
–Lung –Breast –Melanoma –Unknown •Pathology –Often multifocal, at grey-white junction –“Cannon-ball” appearance –Cells from tissue of origin •Treatment: resection for single metastases |
