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Set of slides on brain tumor
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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
1. Tumors of Neuroepithelial Tissue
2. Tumors of Cranial and Spinal Nerves
3. Tumors of the Meninges
4. Tumors of Uncertain Histogenesis1. Hemangioblastoma from primitive vascular structures
5. Lymphomas and Hematopoietic Neoplasm
6. Germ Cell Tumor1. Ex: Germinoma – common in pineal gland area
7. Cysts and Tumor-like lesions1. Usually in the third ventricle
8. Tumors of the Sellar Regions
9. Local Extension from Regional Tumors
10. 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 cannot be 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 most importantly, increased proliferative activity that is reflected as increased mitotic activity.
There should be NO necrosis or endothelial proliferation.
Presence of either/both is suggestive of worse biological behavior.
GLIOBLASTOMA MULTIFORME CSF seeding:
Malignant cells in the CSF may form: a. Distant foci in spinal roots b. White spread meningeal gliomatosis
CSF seeding implies that GBM can go to the CSF spaces such as the subarachnoid space & communicate with the ventricular system
Extraneural metastasis - To bone & lymph nodes (very rare) after a craniotomy
Pseudopalisading around the necrosis is common in GBM
Can cross the midline in a “butterfly” pattern: this shows the aggressive nature of this tumor because the midline is composed of a tough dura
GLIOBLASTOMA MULTIFORME
IMAGING: HIGH- AND LOW-GRADE GLIOMAS High-grade or malignant gliomas: appear as
contrast enhancing mass lesions which arise in white matter & are surrounded by edema
Low-grade gliomas: typically non-enhancing lesions that diffusely infiltrate brain tissue & may involve a large region of 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 the brain
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 brain parenchyma Highly infiltrative May metastasize distantly in ventricular &
subarachnoid spaces 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 obvious attachment 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 cap cells normally seen in arachnoid villi)
20% of all intracranial tumors (with asymptomatic cases—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 from external carotid artery) Hyperostosis of adjacent bone (bone
proliferation)
HISTOLOGICAL CHARACTERISTICS Benign Typical features:
- Whorls of arachnoid cells surrounding a central hyaline material that eventually calcifies to form PSAMMOMA BODIES
- 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) - Falx cerebri - Skull base
- Olfactory groove - Sphenoid ridge - CP angle - Tuberculum sella
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 determining recurrence 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 (or
hyperfunctioning) a. Growth hormone b. Gonadotropin c. Thyroid hormone d. Adrenal hormone e. Prolactin hormone
Macroadenoma - More than 1cm - Symptoms due to compressing normal pituitary
gland and neural structure causing hypofunctioning
PATHOLOGY Endocrine Active (Secretory)
- Prolactinoma - Most common secretory intrasellar endocrine active
tumor - Secreted either by microadenoma or macroadenoma
- 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 CARCINOMAHighly invasiveRapidly growing & anaplasticUnequivocal 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 hemianopsia is the
most common Papilledema is rare May enlarge with pregnancy 5% of pituitary adenoma present with pituitary
apoplexy
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 homonymous
hemianopsia 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
cause accumulation of CSF proximal to the block hydrocephalus
SUPRASELLAR REGION – REGION OF THE HYPOTHALAMUS An example of a suprasellar tumor is a craniopharyngoma
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 until the region of the hypothalamus because visual problems prompt consult & diagnosis.
Papilledema is also rare because it manifests late in the course of the tumor. Before that happens, patient must have been diagnosed already
Obstructive hydrocephalus: rare because of diagnosis at visual 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