brain tumors
TRANSCRIPT
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Brain Tumors
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GLIAL CELLS…….NEURONS
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GLIAL CELLS
Schwann Cell Astrocyte
Microglia Oligodendrocyte
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WHAT IS A BRAIN TUMOR?
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PRIMARY VS. SECONDARY:
May lodge into the ff structures: - Brain parenchyma – most common area of metastases - Leptomeninges – pia mater & arachnoid - Dural space
Primary • originates in the brain.• Children
Secondary
• made up of cells that have spread (metastasized) to the brain from somewhere else in the body.
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Benign
slow-growing
Noncancerous
do not spread to surrounding tissue.
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LOCALIZED VS. INVASIVE
Localized
confined to one area
easier to remove
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THEY CAN ALSO BE:
Extramedullary (Extraaxial)
Meningioma
Pituitary adenoma
Vestibular schwanomma
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WHO GRADING SYSTEM
•Benign cytological features-see below
Grade I-Pilocytic astrocytoma
•Moderate cellularity-no anaplasia or mitotic activity
Grade II-Low-grade astrocytoma
•Cellularity, anaplasia, mitoses Grade III- Anaplastic
astrocytoma
• Same as Grade III plus microvascular proliferation and necrosis
Grade IV-Glioblastoma
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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
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WHAT CAUSES A BRAIN TUMOR?
Being male
Race
AgeFamily history
Occupational
exposures
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OCCUPATIONAL EXPOSURES
Radiation
Formaldehyde
Vinyl chloride
Acrylonitrile
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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.
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AGE INCIDENCE
Adults - Supratentorial: 80-85% - Intratentorial: 15-20%
- Children - Intratentorial: 60% - Supratentorial: 40%
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CLINICAL PRESENTATION
Insidious onset
Headache
Seizure
Mental, behavioral and personality
changes
Lateralizing or focal neurologic deficits
Increased ICP
Slowly Progressive
Tumors
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CEREBRAL DYSFUNCTION
Seizure
Contralateral lesion:Hemiparesis with Babinski reflex & cranial nerve
deficitsHemisensory deficits
Homonymous hemianopsia/quadrantanopsia
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CEREBELLAR DYSFUNCTION
Hemisphere lesion
Ipsilateral limb ataxia
Intention tremor
Dysmetria
Vermis lesion
Dysdiadochokinesia
Truncal ataxia
No limb ataxia
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Brainstem Dysfunction
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INCREASED ICP
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PAPILLEDEMA
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COURSE OF ILLNESS
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ANCILLARY PROCEDURES
Skull X-ray
Neuroimaging studies
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TREATMENT OF BRAIN TUMORS
Surgery
Chemotherapy
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THE NEUROLOGICAL REHABILITATION TEAM:
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Neurologist
Physiatrist
The Rehabilitation Team
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Dietitian
Speech / Language Therapist
The Rehabilitation Team
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COMMON TYPES OF BRAIN TUMORS
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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
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GLIOMAS
Include: a. Astrocytoma b. Oligodendroglioma c. Ependymoma
- WHO Classification Basis a. Increased cellularity b. Nuclear atypia c. Endothelial proliferation d. Necrosis
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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
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GRADE I: Pilocytic Astrocytomas
Primary in children & young adults
Focal astrocytoma may be associated with: Neurofibromatosis type I
(NF-I) Unusually excellent
prognosis
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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
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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
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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.
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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
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GLIOBLASTOMA MULTIFORME
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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.
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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
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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
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OLIGODENDROGLIOMA
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“FRIED EGG CELLS OF OLIGODENDROGLIOMA”
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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
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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
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EPENDYMOMA
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HISTOLOGICAL CHARACTERISTICS OF EPENDYMOMA
Perivascular pseudorosettes
Loss of chromosome 22 particularly 22q
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PROGNOSIS
5-year survival: 40-50% 10-year survival: 47-68% Better prognosis:
Young age Infratentorial Gross total excision Low-grade histology
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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
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MENINGIOMA
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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
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ETIOLOGY OF MENINGIOMA
Radiotherapy
Viral infection (SV-40)
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PROGESTERONE RECEPTORS
- Expressed in 80% of women with meningiomas - Expressed in 40% of men with meningiomas
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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)
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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
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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
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DIAGNOSIS
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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
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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
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SURGERY
Complete excision may cure many meningiomas
The extent of resection is the most important in determining recurrence
For recurrence: reresection
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RADIATION THERAPY
Residual tumor after surgery Recurrent tumor Atypical or malignant histology
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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)
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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
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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
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HISTOLOGICAL CHARACTERISTICS:
Almost all are histologically benign Pituitary CA: rare Macroadenomas Pituitary Carcinoma
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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
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PITUITARY CARCINOMA
Highly invasiveRapidly growing & anaplasticUnequivocal diagnosis relies on
presence of distant metastasis
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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
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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
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VISUAL FIELD PATHWAYS
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BITEMPORAL HEMIANOPSIA
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IPSILATERAL BLINDNESS
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CONTRALATERAL HOMONYMOUS HEMIANOPSIA
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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
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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
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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
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DIAGNOSIS
- X-ray – will show you ballooning of the sella turcica
- Cranial MRI - Best way to evaluate pituitary pathology
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TREATMENT
Surgery
Radiation Treatment
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VIDEO ON ENDOSCOPIC TRANSSPHENOIDAL SURGERY