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Brain tumors
 

Brain tumors

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    Brain tumors Brain tumors Presentation Transcript

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