1. Intracranial Tumours

2. Intracranial neoplasm

3. Intracraneal neoplasm All neoplasms arising from the skull, meninges, blood, blood vessels, pituitary and pineal glands, cranial nerves, brain tissue, or congenital rests, as well as metastatic tumors.

4. General Considerations  Although either benign or malignant, almost all brain tumours are malignant in the sense that they may lead eventually to death if not treated.

5. Epidemiology   Brain tumors are responsible for 2% of all cancer deaths.   The incidence varies with age.   In adults, metastatic brain tumor is the most common intracranial neoplasm comprising about 15-20% of them.   Among the primary, the most frequent are gliomas followed by meningiomas.   Glioma more frequent in males and meningiomas are more common in females.   In children, brain tumors are the second most common after leukemia. 70% are infratentoreal. The most frequent are cerebellar astrocytoma, brainstem glioma, medulloblastoma and ependymoma.   In neonates and in infants, brain tumors are rare mostly congenital.

6. Classification of brain tumours  The classification of brain tumours is determined by their cell of origin.  Over 50% are neuroepithelial in origin, 15% metastatic, 15% meningioma and 8% pituitary tumours.  The World Health Organization (WHO) classification of brain tumours is outlined in the next slide.

7. (WHO) Classification of brain tumours A.Neuroepithelial Tumours: B.Nerve sheath tumour: acoustic neuroma C.Meningeal Tumours: Meningioma D.Pituitary Tumours E.Germ cell tumours: e.g. Germinoma, Teratoma F.Lymphomas G.Tumour-like malformations: H.Metastatic Tumours

8. Neuroepithelial Tumours 1) Gliomas:  Astrocytomas  Oligodendrogliomas  Ependymoma  Choroid plexus tumour 2) Pineal Tumours 3) Neuronal Tumours 4) Medulloblastoma 4) Medulloblastoma

9. Tumour-like malformations 1) Craniopharyngioma 2) Epidermoid tumour 3) Dermoid tumour 4) Colloid cyst

10. Aetiology of Brain Tumors The etiology of brain tumors is still not clearly understood. The etiology of brain tumors is still not clearly understood. Radiation associated with meningioma, glioma and fibrosarcoma Radiation associated with meningioma, glioma and fibrosarcoma Although there is no genetic predisposition, chromosomal abnormalities have been noted in many CNS tumors (e.g. von Recklinghausen's). Although there is no genetic predisposition, chromosomal abnormalities have been noted in many CNS tumors (e.g. von Recklinghausen's). Viruses, EBV associated with Burkitt s lymphoma and nasopharyngeal carcinoma Viruses, EBV associated with Burkitt s lymphoma and nasopharyngeal carcinoma Immunosuppression markedly increase the incidence of primary CNS lymphoma. Immunosuppression markedly increase the incidence of primary CNS lymphoma. Mutation in the p53 tumor suppressor gene is the most common gene alteration and is found in astrocytoma and meningioma Mutation in the p53 tumor suppressor gene is the most common gene alteration and is found in astrocytoma and meningioma

11. Clinical Features of Brain Tumours This will result from one or a combination of: This will result from one or a combination of: a) Focal neurological deficits b) Raised intracranial pressure c) Seizures, and d) Endocrine dysfunction, or e) Incidental findings (i.e. symptomless).

12. a) Focal Neurological Deficits 1.Frontal lobe lesions: presents with personality changes, gait ataxia, and urinary incontinence, contralateral hemiparesis if posterior frontal and expressive dysphasia if involving the dominant inferior frontal gyrus. 2.Parietal lobe lesions: contralateral sensory impairement, dressing apraxia, asteriognosis and, if on the dominant side, acalculia, agraphia, left-right disorientation and finger agnosia. 3.Temporal lobe lesions: olfactory and auditory hallucination, memory disturbances, contralateral superior quadrantanopia or hemiparesis and, if on the dominant side, receptive dysphasia. 4.Occipital lesions: associated with visual field deficits, most commonly an incomplete contralateral homonymous hemianopia.

13. a) Focal Neurological Deficits 5. Subfrontal lesions: may involve the olfactory nerves (anosmia). 6. Sellar and parasellar: tumours present with visual field problems due to compression of the optic chiasm, hypopitutarism and oversecretion syndromes such as Cushing's disease and acromegaly. 7. Cerebellar lesions: Tumours involving the cerebellar vermis cause truncal ataxia, whereas tumours in the hemispheres produce appendicular signs such as incoordination and nystagmus. 8. Brainstem and Cerebellopontine angle lesions: may result in cranial nerve palsies, long tract signs and secondary hydrocephalus. 9. Ventricular system tumours: may obstruct CSF drainage and result in hydrocephalus, compounding raised ICP.

14. b) Raised Intracranial Pressure 1. Direct mass effect. 2. Vasogenic oedema. 3. Obstructive hydrocephalus.

15. c) Seizures New onset of seizure in an adult is suggestive of an intracranial mass until proven otherwise. New onset of seizure in an adult is suggestive of an intracranial mass until proven otherwise. The type of seizure may give a clue to the location of the tumour: The type of seizure may give a clue to the location of the tumour: Parietal lesions cause simple partial seizures, which may become secondarily generalized. Parietal lesions cause simple partial seizures, which may become secondarily generalized. Medial temporal lesions will cause complex partial seizures. Medial temporal lesions will cause complex partial seizures.

16. c) Seizures Late onset epilepsy, particularly over the age of 30 years, should prompt investigations to exclude an intracranial neoplasm. Late onset epilepsy, particularly over the age of 30 years, should prompt investigations to exclude an intracranial neoplasm. New onset of seizure in an adult is suggestive of an intracranial mass until proven otherwise. New onset of seizure in an adult is suggestive of an intracranial mass until proven otherwise. The type of seizure may give a clue to the location of the tumour: The type of seizure may give a clue to the location of the tumour: Parietal lesions cause simple partial seizures, which may become secondarily generalized. Parietal lesions cause simple partial seizures, which may become secondarily generalized. Medial temporal lesions will cause complex partial seizures. Medial temporal lesions will cause complex partial seizures.

17. Personality Changes

18. Headache

19. Vomiting

20. Papilloedema

21. Ataxia

22. Investigations of Brain Tumours 1. Plain Skull x-ray 2. Computed Tomography (CT-scan) 3. Magnetic Resonance Imaging (MRI) 4. Angiography 5. Positron Emission Tomography (PET).

23. Investigations of Brain Tumours I.Plain Skull x-ray: I.Plain Skull x-ray: a.May be normal a.May be normal b.May show changes due to raised intracranial pressure. b.May show changes due to raised intracranial pressure. c.Local changes may occur with specific tumours: like c.Local changes may occur with specific tumours: like 1.Suprasellar calcification in craniopharyngiomas 1.Suprasellar calcification in craniopharyngiomas 2.Hyperostosis and skull thickening in meningioma. 2.Hyperostosis and skull thickening in meningioma.

24. Investigations of Brain Tumours Computed Tomography (CT-scan): Computed Tomography (CT-scan): 1.Site and size of the tumour. 2.Boundaries of the tumour. 3.If there is surrounding oedema or not. 4.Shift of the midline structures by the mass. 5.Associated hydrocephalus. 6.Bony changes. 7.Nature of the tumour (solid, cystic, necrotic or calcified), and so its pathology.

25. Investigations of Brain Tumours 3. Magnetic Resonance Imaging (MRI): same as CT 4. Angiography: Used to evaluate the blood supply and vasculature of the tumor.

26. Investigations of Brain Tumours 5. Positron Emission Tomography (PET): can study the brain metabolism.   Used to characterize the most malignant component of a tumour.   Assess prognosis of brain tumour.   Differentiate recurrent tumour from radiation necrosis.

27. Management of intracranial tumours 1.If the patient shows signs of compression, or raised intracranial pressure, treat with measures that lower ICP. 2.If an intracranial tumour is associated with hydrocephalus, the hydrocephalus is dealt with first by a ventriculoperitoneal shunt before surgery. 3. CT or MRI guided stereotactic surgery : tumour is deeply seated in the brain. 4. Surgical excision or debulking for accesssible tumours. 5. In cases of malignant brain tumours or metastases : adjunctive therapy : Radiotherapy and/or Chemotherapy are supplementary to surgical excision.

28. Management of intracranial tumours a. a.Radiotherapy either conventional radiotherapy or radiosurgery For small tumor less than 3 cm which is of many types i. i. Linear accelerator ii. ii. Gama knife iii. iii. Cyber knife

30. Cyber knife

31. Stereotactic Neurosurgery

32. Metastatic Brain Tumours Constitute 15% of intracranial tumours. Constitute 15% of intracranial tumours. The commonest sites of origin are the lung (40%) and breast (10-30%), in addition to melanoma (5- 15%), kidney and colon. The commonest sites of origin are the lung (40%) and breast (10-30%), in addition to melanoma (5- 15%), kidney and colon. In 15% of cases, a primary source is never found. In 15% of cases, a primary source is never found. On CT, they only show well with intravenous contrast. On CT, they only show well with intravenous contrast. Steroids may help reduce peritumour oedema. Steroids may help reduce peritumour oedema. Surgery may be appropriate for an isolated metastasis. Surgery may be appropriate for an isolated metastasis. CSF shunt used for lesions causing Hydrocephalus. CSF shunt used for lesions causing Hydrocephalus. Radiotherapy can be used for multiple metastases. Radiotherapy can be used for multiple metastases.

33. Metastatic Brain Tumours

34. Metastatic Brain Tumours Pre contrast CT

35. Metastatic Brain Tumours Post contrast CT

36. Metastatic Brain Tumours MRI

38. Gliomas They are derived from cells of glial origin. They are derived from cells of glial origin. They are the commonest of primary CNS neoplasms. They are the commonest of primary CNS neoplasms. They form 50% of adult intracranial tumours.They form 50% of adult intracranial tumours. They are of four types: astrocytoma, oligodendroglioma, ependymoma and choroid plexus papilloma. The most common of which is astrocytoma.They are of four types: astrocytoma, oligodendroglioma, ependymoma and choroid plexus papilloma. The most common of which is astrocytoma. Survival is closely associated with grading.Survival is closely associated with grading. Treatment involves surgery and radiotherapy and/or chemotherapy.Treatment involves surgery and radiotherapy and/or chemotherapy.

39. Glioma

40. Astrocytoma

41. Astrocytoma Pre contrast CT

42. Astrocytoma Post contrast CT

43. Astrocytoma Pre contrast MRI

44. Astrocytoma Post contrast MRI

45. Malignant Glioma Pre contrast CT

46. Malignant Glioma Post contrast CT

47. Meningiomas These account for 15% of intracranial neoplasms, and are the most common benign neoplasm.These account for 15% of intracranial neoplasms, and are the most common benign neoplasm. They occur more frequently in women than in men, and their incidence peaks in middle age.They occur more frequently in women than in men, and their incidence peaks in middle age. The tumour arises from meningothelial cells of the arachnoid villi.The tumour arises from meningothelial cells of the arachnoid villi.

48. Meningiomas They classically arise from a broad base along the dura. They classically arise from a broad base along the dura. They may invade bone.They may invade bone. They derive their blood supply from the external carotid circulation.They derive their blood supply from the external carotid circulation. Malignant meningiomas are relatively rare.Malignant meningiomas are relatively rare. The symptoms and signs are related to those of intracranial mass lesions or seizures.The symptoms and signs are related to those of intracranial mass lesions or seizures. CT scan accurately diagnoses the lesions.CT scan accurately diagnoses the lesions. Complete surgical removal usually results in cure.Complete surgical removal usually results in cure.

49. Meningioma Pre contrast CT

50. Meningioma Post contrast CT

51. Meningioma Pre contrast MRI

52. Meningioma Post contrast MRI

53. Meningioma Bone Involvement

55. Pituitary Tumours Non-functioning pituitary adenomas Non-functioning pituitary adenomas Functioning pituitary adenomas Functioning pituitary adenomas

56. Non-functioning pituitary adenomas 1. Accounts for about 30% of pituitary tumours. 2. They are often seen in the fourth and fifth decades of life. 3. Because they are non-functioning, they are not generally diagnosed until they are very large. 4. Their presentation is by optic chiasm compression that cause visual field defect (bitemporal hemianopia). 5. The usual treatment is microscopic trans- sphenoidal or trans-cranial excision.

57. Functioning pituitary adenomas 1. Pituitary adenomas are classified according to the hormones they secrete. They include: i.Prolactin secreting adenomas. ii.Growth hormone secreting adenomas that produce acromegaly or gigantism. iii.Glycoprotein secreting adenomas that produce excess amount of TSH, LH, or FSH. iv.ACTH secreting adenomas that produce Cushing's disease. v.Some of these secrete more than one hormone, e.g. prolactin-growth hormone secreting adenomas.

58. Functioning pituitary adenomas 2. Adenomas may be further divided according to their sizes into Microadenomas that are less than 1 cm in diameter, and Macroadenomas that have a larger size. 3. Functioning adenomas are diagnosed by: i. Clinical changes. ii. Hormone assessment. And iii. Radiology by using MRI and CT scan.

59. Functioning pituitary adenomas 4. Prolactinomas represent 40% of all pituitary adenomas. They cause amenorrhoea, galactorrhoea, and infertility in women, while in men they cause impotence or may be asymptomatic. 5.Bromocriptin (antiprolactin drug) has virtually replaced surgery as the treatment of choice for prolactinomas. 6.Surgical excision can preferably done by using the trns-sphenoidal route, whether sublabial or transnasal, although transcranial approach can also be used. 7.In case of an invasive tumour with incomplete excision, radiotherapy is required

61. Trans sphenoidal

62. DO NOT FORGET 1. The most significant findings pointing to an intracranial tumour on physical examination are the presence of papilloedema and signs of focal damage to the nervous system. 2. If a cerebral tumour is suspected, LUMBAR PUNCTURE IS CONTRAINDICATED as it may precipitate a fatal coning of the brain stem through the foramen magnum.

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