Brain tumors


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Brain tumors

  1. 1. Brain Tumors<br />
  2. 2. Glial Cells…….Neurons<br />
  3. 3. Glial Cells <br />
  4. 4.
  5. 5. What Is a Brain Tumor?<br />
  6. 6. Primary vs. secondary: <br />May lodge into the ff structures:<br />- Brain parenchyma – most common area of metastases<br />- Leptomeninges – pia mater & arachnoid<br />- Dural space<br />
  7. 7.
  8. 8. Localized vs. invasive<br />
  9. 9. THEY CAN ALSO BE:<br />
  10. 10. WHO GRADING SYSTEM<br />
  11. 11. WHO Histologic Classification of Tumors of the CNS<br />Tumors of Neuroepithelial Tissue<br />Tumors of Cranial and Spinal Nerves<br />Tumors of the Meninges<br />Tumors of Uncertain Histogenesis<br />Hemangioblastoma from primitive vascular structures<br />Lymphomas and Hematopoietic Neoplasm<br />Germ Cell Tumor<br />Ex: Germinoma – common in pineal gland area<br />Cysts and Tumor-like lesions<br />Usually in the third ventricle<br />Tumors of the Sellar Regions<br />Local Extension from Regional Tumors<br />Metastatic Tumors<br />
  12. 12. What Causes a Brain Tumor?<br /> <br />
  13. 13. Occupational exposures<br />
  14. 14. Common Types of Brain Tumors<br /><ul><li>Astrocytomas come in four major subtypes:
  15. 15. juvenile pilocytic astrocytoma (grade 1)
  16. 16. fibrillary astrocytoma (grade 2)
  17. 17. anaplastic astrocytoma (grade 3)
  18. 18. glioblastoma multiforme (grade 4)
  19. 19. The higher the grade, the more aggressive the tumor.</li></li></ul><li>Age Incidence<br />Adults<br />- Supratentorial: 80-85%<br />- Intratentorial: 15-20%<br />- Children<br />- Intratentorial: 60%<br />- Supratentorial: 40%<br />
  20. 20. Clinical Presentation<br />Slowly <br />Progressive <br />Tumors<br />
  21. 21. Cerebral Dysfunction<br />
  22. 22. Cerebellar Dysfunction<br />
  23. 23.
  24. 24. Increased ICP<br />
  25. 25. Papilledema<br />
  26. 26. Course of Illness<br />
  27. 27. Ancillary Procedures<br />
  28. 28. Treatment of Brain Tumors<br />
  29. 29. The Neurological Rehabilitation team:<br />
  30. 30. The Rehabilitation Team<br />
  31. 31. The Rehabilitation Team<br />
  32. 32. Common types of brain tumors<br />
  33. 33. I. GLIOMAS<br />- Most common primary brain tumor<br />- 50% of all symptomatic brain tumors<br />- Incidence increases with advancing age<br />- Peak in 8th and 9th decades<br />- No known environmental factors<br />- No behavioral lifestyle choices<br />- Ionizing radiation: the only clear risk factor<br />- Originate from glial cells or their stem cell precursors<br />
  34. 34. GLIOMAS<br />Include:<br />a. Astrocytoma<br />b. Oligodendroglioma<br />c. Ependymoma<br />- WHO Classification Basis<br />a. Increased cellularity<br />b. Nuclear atypia<br />c. Endothelial proliferation<br />d. Necrosis<br />
  35. 35. A. Astrocytoma<br />- Most common glioma<br />- Cerebral astrocytoma (more in adults)<br />- Behavioral changes<br />- Seizures<br />- Hemiparesis<br />- Language difficulty<br />- Cerebellar astrocytoma (more in children)<br />- Hemisphere<br />- Ataxia<br />- Brain stem (children)<br />- Pons<br />- CN deficits<br />
  36. 36. Grade I: <br />Pilocytic Astrocytomas<br />Primary in children & young adults<br />Focal astrocytoma may be associated with:<br />Neurofibromatosis type I (NF-I)<br />Unusually excellent prognosis<br />
  37. 37. Grade II: <br />Diffuse or Fibrillary Astrocytoma<br />Most common in the cerebral hemisphere in young adults<br />Low grade or benign histologically<br />Infiltrative – usually a problem because the tumor cannotbe resected completely if this is a characteristic of the tumor<br />Complete resection not possible<br />Latent potential for malignant transformation<br />
  38. 38. Grade III: Anaplastic AstrocytomaGrade IV: Glioblastoma multiforme<br />Grades III and IV are high-grade gliomas<br />20% of all intracranial tumors<br />55% of gliomas<br />80% of gliomas of the cerebral hemispheres in adults<br />Peak incidence middle to late adulthood<br />Males/females = 1.61<br />No familial predilection<br />
  39. 39. Anaplastic Astrocytoma<br />Have increased pleomorphism, enlarged nuclei and mostimportantly, increased proliferative activity that is reflectedas increased mitotic activity.<br />There should be NO necrosis or endothelial proliferation.<br />Presence of either/bothis suggestive of worse biologicalbehavior.<br />
  40. 40. Glioblastoma Multiforme<br />CSF seeding:<br />Malignant cells in the CSF may form:<br />a. Distant foci in spinal roots<br />b. White spread meningealgliomatosis<br />CSF seeding implies that GBM can go to the CSFspaces such as the subarachnoid space &communicate with the ventricular system<br />Extraneural metastasis<br />- To bone & lymph nodes (very rare) after a craniotomy<br />Pseudopalisadingaround the necrosis is common in GBM<br />Can cross the midline in a “butterfly” pattern: this shows theaggressive nature of this tumor because the midline iscomposed of a tough dura<br />
  41. 41. Glioblastoma Multiforme<br />
  42. 42. Imaging: High- and Low-Grade Gliomas<br />High-grade or malignant gliomas: appear as contrast enhancingmass lesions which arise in white matter & aresurrounded by edema<br />Low-grade gliomas: typically non-enhancing lesions thatdiffusely infiltrate brain tissue & may involve a large regionof brain<br />Low-grade gliomas are usually best appreciated on T2-weighted MRI scans.<br />
  43. 43. Prognosis of Astrocytomas<br />Median survival<br />GBM: 1 year<br />Anaplastic astrocytoma: 3 years<br />Low-grade astrocytoma: 5 years<br />Others survive a decade or more<br />Most die from transformation of tumor to higher grade<br />
  44. 44. B. Oligodendroglioma<br />Derived from oligodendrocytes or their precursors<br />Oligodendrocytes produce the white matter in thebrain<br />5-7% of all intracranial gliomas<br />Most often in the 3rd and 4th decades<br />Males:females = 2:1<br />Found primarily in cerebral hemispheres, within the brainparenchyma<br />Highly infiltrative<br />May metastasize distantly in ventricular & subarachnoidspaces like the GBM (CSF seeding)<br />Round regular “fried-egg” cells<br />
  45. 45. Oligodendroglioma<br />
  46. 46. “fried egg cells of oligodendroglioma”<br />
  47. 47. Prognosis of Oligodendroglioma<br />Median Survival<br />Low-grade oligodendrogliomas: 8-16 years<br />Anaplastic oligodendrogliomas: 5 years<br />Tumors that have 1p/19q LOH—best prognosis<br />Many pxs die from malignant transformation of the tumor<br />
  48. 48. C. Ependymoma<br />Arise from ependymal cells (an intraventricular tumor)<br />More common in children<br />10% pediatric intracranial tumors<br />5% of adult intracranial tumors<br />Most common in the 4th ventricle<br />Ataxia, vertigo, increased ICP<br />May grow in brain parenchyma without obviousattachment to the ventricular system<br />Spinal lesions more common in adults<br />Intracranial ependymomas predominate in children<br />
  49. 49. Ependymoma<br />
  50. 50. Histological Characteristics of Ependymoma<br />
  51. 51. Prognosis<br />5-year survival: 40-50%<br />10-year survival: 47-68%<br />Better prognosis:<br />Young age<br />Infratentorial<br />Gross total excision<br />Low-grade histology<br />
  52. 52. II. MENINGIOMA<br />Second most common primary brain tumor<br />Originate from arachnoid cells (meningoepithelial capcells normally seen in arachnoidvilli)<br />20% of all intracranial tumors (with asymptomaticcases—40% or more)<br />7% of all posterior fossa tumors<br />3-12% of cerebellopontine angle tumors<br />
  53. 53. MENINGIOMA<br />
  54. 54. II. MENINGIOMA<br />Most diagnosed in 6th % 7th decades<br />Female: Male—3:2 to 2:1<br />Multiple in 5-15% (NF-2)<br />90% intracranial<br />10% intraspinal<br />Spinal meningioma: 10x in women<br />All familial meningiomas occur with NF-2<br />Rare in children (more in boys)<br />- Rare with dural attachments<br />- Usually Intraventricular or posterior fossa<br />- Commonly with sarcomatous changes<br />- Frequently with NF-2<br />
  55. 55. Etiology of Meningioma<br />
  56. 56. Progesterone receptors<br />- Expressed in 80% of women with meningiomas<br />- Expressed in 40% of men with meningiomas<br />
  57. 57. Pathology<br />Nodular tumors occasionally meningiomas en plaque(sheer-like formation)<br />Highly vascular<br />Encapsulated and attached in the dura (blood supply fromexternal carotid artery)<br />Hyperostosis of adjacent bone (bone proliferation)<br />
  58. 58. Histological Characteristics<br />Benign<br />Typical features:<br />- Whorls of arachnoid cells surrounding a central hyalinematerial that eventually calcifies to form PSAMMOMABODIES<br />- No characteristic cytologic marker<br />
  59. 59. Clinical Manifestations<br />Some are asymptomatic—found incidentally by MRI<br />But may have symptoms:<br />Tumor location: by compression of underlying neural structures<br />Sites of predilection<br />- Cerebral convexity (Sylvian & parasagittal areas)<br />- Falxcerebri<br />- Skull base<br />- Olfactory groove<br />- Sphenoid ridge<br />- CP angle<br />- Tuberculumsella<br />
  60. 60. diagnosis<br />
  61. 61. diagnosis<br />Cranial CT Scan<br />Isointense or slightly hyperintense<br />Hyperostosis—20%<br />Isointense (65%) or hypointense (35%) in T1 and T2<br />Gadolinium <br />Angiography<br />Hypervascular mass<br />embolization reduce the risk of intraoperative bleeding<br />MR Angiography & Venography<br />
  62. 62. Growth Rate of Meningioma<br />Less than 1 cm per year (very slow growth but can recur)<br />Tumor doubling time: 1.27 to 14.35 years<br />
  63. 63. Surgery<br />Complete excision may cure many meningiomas<br />The extent of resection is the most important in determiningrecurrence<br />For recurrence: reresection<br />
  64. 64. Radiation Therapy<br />Residual tumor after surgery<br />Recurrent tumor<br />Atypical or malignant histology<br />
  65. 65. III. TUMORS OF THE PITUITARY GLAND<br />Third most common primary<br /> brain tumor<br />Often asymptomatic<br />Incidence at autopsy: <br />1.7 – 24%<br />Most common in adults in <br />the 3rd and 4th decade<br />10% incidence in children & adolescents<br />Not hereditary except MEN-1 (multiple endocrine neoplasia)<br />
  66. 66. Pathology<br />Microadenoma<br />- Less than 1cm<br />- Symptoms due to excess hormone secretion (orhyperfunctioning)<br />a. Growth hormone<br />b. Gonadotropin<br />c. Thyroid hormone<br />d. Adrenal hormone<br />e. Prolactin hormone<br />Macroadenoma<br />- More than 1cm<br />- Symptoms due to compressing normal pituitary glandand neural structure causing hypofunctioning<br />
  67. 67. Pathology<br />Endocrine Active (Secretory)<br />- Prolactinoma<br />- Most common secretoryintrasellar endocrineactive tumor<br />- Secreted either by microadenoma ormacroadenoma<br />- Growth hormone<br />- Before closure of epiphysis ® gigantism<br />- After closure of epiphysis ® acromegaly<br />- ACTH: Cushing’s Syndrome<br />- FSH and LH<br />- Endocrine Inactive (Non-secretory or null cell adenoma)<br />- 10% mixed secretory tumor<br />
  68. 68. Histological characteristics:<br />Almost all are histologically benign<br />Pituitary CA: rare<br />Macroadenomas<br />Pituitary Carcinoma<br />
  69. 69. Macroadenomas<br />May invade dural bone<br />May infiltrate surrounding structure<br />Locally invasive pituitary adenomas are nearly always histologically benign<br />Pleomorphism and mitotic figure insufficient for diagnosis of carcinoma (may be seen in benign adenomas)<br />Invasive character independent of growth rate<br />
  70. 70. Pituitary Carcinoma<br />Highly invasive<br />Rapidly growing & anaplastic<br />Unequivocal diagnosis relies on presence of distant metastasis<br />
  71. 71. Clinical Manifestations of Tumors of the Pituitary Gland<br />Compression of neural and vascular structures<br />Headache<br />Hypopituitarism<br />Visual symptoms<br />- visual loss<br />- visual field abnormality: bitemporal hemianopsiais the most common<br />Papilledema is rare<br />May enlarge with pregnancy<br />5% of pituitary adenoma present with pituitaryapoplexy<br />
  72. 72. Clinical Manifestations of Tumors of the Pituitary Gland<br />Optic chiasm<br />- Between hypothalamus & sella turcica<br />- When this is compressed ® bitemporal hemianopsia<br />Optic nerve<br />- When this is compressed ® ipsilateral blindness<br />Optic tract<br />- When this is compressed ® contralateral homonymoushemianopsia<br />Diaphragma sella<br />- The dura that covers sella turcica<br />As tumor grows forward to the sella ® compress the basal dura ® headache ® affected pain-sensitive intracranial structures<br />- Basal dura is a pain-sensitive intracranial structure<br />
  74. 74. bitemporal hemianopsia<br />
  76. 76. contralateral homonymous hemianopsia<br />
  77. 77. Hypothalamus + thalamus<br />- Form the lateral wall of the 3rd ventricle<br />- Any pathology in the ventricular system will causeaccumulation of CSF proximal to the block ®hydrocephalus<br />
  78. 78. Suprasellar region – region of the hypothalamus<br />An example of a suprasellar tumor is acraniopharyngoma in children & adults<br />A craniopharyngoma can compress the third ventricle &cause the ff: (hydrocephalus with signs of increased ICP)<br />- Headache<br />- Vomiting<br />- Papilledema<br />Nowadays, pituitary adenoma usually does not grow untilthe region of the hypothalamus because visual problemsprompt consult & diagnosis.<br />Papilledema is also rare because it manifests late in thecourse of the tumor. Before that happens, patient musthave been diagnosed already<br />Obstructive hydrocephalus: rare because of diagnosis atvisual problem level<br />
  79. 79. Pituitary Apoplexy<br />- Hemorrhage or infarction of pituitary adenoma<br />- Sudden onset of headache, nausea, vomiting, visual loss,diplopia, altered mental status<br />- Diagnosis by CT or MRI<br />- Treatment emergency surgery<br />
  80. 80. Diagnosis<br />- X-ray – will show you ballooning of the sella turcica<br />- Cranial MRI<br />- Best way to evaluate pituitary pathology<br />
  81. 81. Treatment<br />
  82. 82. Video on Endoscopic Transsphenoidal Surgery<br />