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Astrocytoma
Most common primary intra-axial brain tumor
12,000 cases/year Classification:
1.fibrillary
2.gemistocytic3.protoplasmic
4.pilocytic
5.microcystic cerebellar
CNS tumors
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SPREAD
-tracking through the white matter(corpus
callosum,cerebral peduncles,centrum
semiovale,internal capsule)
-CSF pathways
-rarely spread systematically
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Neuropathological Grading (WHO)
Characteristic Astrocyto.
(Gr.I)
Anaplastic
Astrocyto.
(Gr.II)
GBM
(Gr.III)
hypercellularity slight
moderate mod.-
marked
pleomorphism slight moderate mod.-marked
Vascularproliferation
none permitted common(not req.)
necrosis none none required
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Neuroradiological Grading
Grade CT features MR findings
I Low density,no mass
effect
Abnormal signal,no
mass effect
II Low density + masseffect
Abnornal signal +mass effect
III Complex enhancement
IV Necrosis(ring enhancement)
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Approximate survival (Astrocytoma)
Grade Median survival
I 8-10 yrs
II 7-8 yrs
III 2 yrs
IV
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Low grade astrocytoma
tend to occur in children and young adults
demonstrate low deg.of cellularity
calcifications are rare, mitosis are absent
0.7-16% among astrocytoma
young agegood prognosticator
increased ICP,altered conciousness,personality
change,significant neurologic deficit=poorprognosis
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treatment
Gross total excision if feasible
surgery is not curative for most infiltratinghemispheric gliomasdue to its characteristic whichextend at least 2 cm into the normal brain
Seizure control 15-75% will undergo malignant degeneration in 5
years
Relieve pressure from large tumors threateningwith hernation
Relieve obstruction of csf pathway
Post op Radiation for grade II astrocytomas
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High grade astrocytoma (grade III and IV)
Anaplastic astrocytoma:
mean age:46 yrsmean duration of symp:15.7mos.
Glioblastoma multiforme:
mean age:56 yrs
mean duration of symp:5.4mos
GBM most common primary brain tumor
most malignant(kernohan IV) histological feature:
neovascularization with endothelial proliferation
areas of necrosis
pseudopallisading around area of necrosis
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GBM
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AA GBM
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Treatment
Functional surgery Tumor debaulking/ cytoreduction
Prolong survival
External beam radiation Chemotherapy
Stereotactic biopsy:
1.eloquent/inaccessible2.small tumors
3.dx.
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Cerebellar Astrocytoma
often cystic,half have mural nodule
better prognosis than supratentorial mean age of occurrence is lower
27% of pediatric p-fossa tumors
postop.survival longer
Presentation:
usually those of any p-fossa mass (ataxia, hydrocephalus,
cerebellar signs)
Pathology:
-solid/cystic(proteinaceous fluid)
-50% have mural nodule,cyst lining of reactive,non-neoplastic tissue
Prognosis:
10yr survival=94%
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Treatment
Excision
Surveillance for recurrence
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Oligodendroglioma-frequently presents with seizure
-often calcified
-predilection in the frontal lobes- fried egg appearance on microscopy
- 4% of primary brain tumors
- Average age =40yrs
- Male:female(60:40)
Presentation:
-50-80% -seizure
-often related to mass effect and less commonly to inc.ICP
Pathology:
-cells with monotonous round nuclei often in cellular sheets
-fried egg-lucent perinuclear halo
-16% of hemispheric ODG are cystic
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Treatment
Gross total resection if possible
Chemotherapy
Radiation therapy
Prognosis:
10 yr=10-30%
-frontal lobe ODG survived longer
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Meningiomas slow growing,extra-axial,usually benign
arise from arachnoid falx,convexity,sphenoid bone
cause hyperostosis of adjacent bone
freq.calcified
classic pathological finding:psammoma bodies multiple in 8% of cases
Meningioma en plaque=diffuse type
-14.3-19% of primary intracranial neoplasm
-peak incidence=45 years-F:M(1.8:1)
-1.5%=childhood
-19-24%=adolescent
-60-70%=falx,convexity,sphenoid bone
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Parasagittal and falx meningiomas
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Parasagittal and falx meningiomas:
half invade the superior sagittal sinus
manifest.=motor difficulty with the contralateral foot
Olfactory groove meningioma: foster-kennedy syndrome
mental status changes
urinay incontinence
visual impairment Seizure
Pathological Classification:
1.meningotheliomatous/syncitial
-sheets of polygonal cells
2.fibrous or fibroblastic
-cells separated by connective tissue stroma
3 t iti l
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3.transitional
-contains whorls,some of which are calcified(psammoma bodies)
4.angiomatous-meningotheliomatous variety with closely packedblood vessels
5.angioblastic-meningeal hemangiopericytoma
6.malignant
-characterized by frequent mitoses,cortical
invasion,metastases
Most common site of mets:
Lung,liver,lymph nodes and heart
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treatment
Surgery
Total excision
Recurrence:
Gross total excision=11-15% in 10 years
Incomplete= 59% in 5 years
Recurrence:Gross total excision=11-15%
Incomplete=29%
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SIMPSON GRADING
I=macroscopically complete
II=macroscopically complete+coagulationIII=macroscopically complete without coag.or dural
excision
IV=partial removal
V=simple decompression
Value of XRT
Recurrence rate
total resection:4%
partial resection without XRT:60%
partial resection with XRT:32%
ACOUSTIC NEUROMA
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ACOUSTIC NEUROMA
are really schwannomas
superior vestibular division of the 8th nerve
3 common early symptoms: hearing loss(98%)
tinnitus(70%)
dysequilibrium(67%)
8-10%
Antoni A fibers
-narrow and bipolar cells
Antoni B fibers
-loose reticulated
arise from loss of a tumor suppressor gene on the long arm ofchrom.22
Neurofibromatosis type 2
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Neurofibromatosis type 2
inc.incidence
bilateral AN
Symptoms:
Unilateral sensorineural hearing loss,tinnitus,dysequilibrium(VIII)
Otalgia,facial numbness and weakness,taste changes (V,VII)
Brain stem compressionSigns:
VII-earliest cranial invloved
Rinne test-positive
Weber test-lateralized to side of better hearing
other signs:abnormal corneal reflex,nystagmus,facialhypoesthesia,facial weakness,abnormal eye movement,papilledema,babinski sign
Radiographic evaluation:
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Radiographic evaluation:
MRI
-diagnostic procedure of choice
-sensitivity:98%-0% false positive rate
-char.=round or oval enhancing tumor centered on IAC
CT scan
-second choice
-normal in 6%
-advantage over MRI:shows bony anatomy- trumpeting-enlarge IAC ostium
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Treatment
Excision
Radiation
Gamma knife surgery
ACOUSTIC NEUROMA
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ACOUSTIC NEUROMA
Cranial nerve preservation in suboccipital removal
Size of tumor Preserved function
VII nerve VIII nerve
2 cm 50-76% 6%
Complications(morbidity/mortality)
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Complications(morbidity/mortality)
meningits-5.7%
CSF leaks-7.2%
CVA-0.7%
shunt req.-0.7%
Cranial nerve dysfx.=VII, VIII,IX,X,XIIbrainstem dysfx.
Follow-up
-CT-scan,MRI
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PITUITARY ADENOMA
-arise primarily from the adenohypophysis
-10% of the intracranial tumors
-most common in the 3rd and 4th decades of life
-affect both sexes equally
-incidence inc.in MEN/MEA
Microadenoma=< 1cm
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Presentation:
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Presentation:
-endocrine disturbance
-mass effect
-pituitary apoplexy-CSF rhinorrhea
*Pituitary apoplexy=abrupt onset of neurologicdeterioration(HA,visualdist.,opthalmoplegia,reduced mental status)
-Hge. and/necrosis(3% of macroade.)
Classified:
1.Functional
2.Non-functional
Functional Pituitary Tumors:
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Functional Pituitary Tumors:
Hormone secreted
1.ACTH/corticotropin
a.endogeneous hypercoticolism(cushings dse)
b.Nelsons syndrome
2.Prolactin
-amenorrhea-galactorrhea
-impotence
-infertility
3.Growth hormone
-acromegaly in adults
-gigantism in prepubertal children
Non-Functional Pituitary Tumors:
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Non Functional Pituitary Tumors:
Manifestation:
1.visual disturbance-bitemporal hemianopsia(opticchiasm)
2.hypopituitarism
3.cavernous sinus
4.prolactin levels(ng/ml)
150=prolactinoma
5.posterior pituitary
check adequacy of ADH
*Dexamethasone suppression test
Endocrine evaluation
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Endocrine evaluation
-may give indication of tumor type
-needs hormone to be replaced
-comparison following treatment1.Adrenal axis
-cortisol
2.thyroid axis
-T4,TSH
3.gonadal axis
-FSH,LH,sex steroids(estradiol,testoterone)
ACROMEGALY
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ACROMEGALY
1.growth hormone
>10ng/ml
2.borderline cases
somatomedine-C (IGF-I)
glucose suppression test
growth hormone releasing hormone stimulation test
3.PRL
PITUITARY TUMORS
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U U O S
Radiographic evaluation:
MRI-imaging of choice
-information about invasion of cav. sinus-location/inv.of parasellar carotids
CT
Contrast enhancement:(time dependent)
1.normal pituitary
2.macroadenomas enhance more
3.microadenomas enhance less
Angiography-localize the parasellar carotids
Treatment
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Treatment1.Acromegaly
surgery
medical tx:bromocriptine,octreotideradiation
Medical
1.bromocriptine2.Octreotide
Radiation
-not routinely useSurgery
PITUITARY TUMORS
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PITUITARY TUMORS
Indications for surgery
1.prolactinomas
2.primary cushings dse.
3.acromegaly
4.macroadenomas5.pituitary apoplexy
6.histopathologic dx
*Diabetic Insipidus
PITUITARY TUMORS
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Post-op. comlications:
1.hypopituitarism
2.secondary empty-sella syndrome3.infection-pituitary abscess,meningitis
4.CSF rhinorrhea
5.Carotid artery rupture
6.nasal septum perforation
Outcome(transphenoidal surgery)
endocrinologic cureprolactinoma=25%
growth hormone=20%
Gross total unusual in tumors>2cm
recurrence=12%
CRANIOPHARYNGIOMA
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CRANIOPHARYNGIOMA-arise from anterior superior margin of the pituitary
-lined with with stratified squamous epithelium-solid and cystic component
-cholesterol crystal
-calcification (50%)
-2.5%-4%
-50%occur in childhood(5-10yrs)
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CRANIOPHARYNGIOMA
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CRANIOPHARYNGIOMA
Treatment:
surgery
outcome=5-10% mortality
5 year survival=55-85%
Radiationcontroversial
Recurrence
most occur in
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CRANIOPHARYNGIOMA
Comparison of Craniopharyioma:Rathkes cleft cyst
Feature Craniopharyngio. Rathkes cleft cyst
Site of origin Anterior superior
margin of pit.
Pars intermedia of
pit.Cell lining Stratified
squamous epith.Single layer
cuboidal epith.
Cysts contents Cholesterolcrystals
Resembles motoroil
Surgical
treatment
Total removal Partial excision
And drainage
CEREBRAL METASTASIS
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CEREBRAL METASTASIS-most common brain tumor seen clinically
-15-20% of patient with Ca
-15% as initial presenting symptom in pt.with no CA hx.
-43-60% will have an abnormal CXR
CEREBRAL METASTASIS
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CEREBRAL METASTASIS
Incidence inc.:
1.increasing length of survival
2.enhanced ability to diagnose CNS tumors
3.many chemotherapeutic agents cant cross the BBB
4.some chemotx.agent weakens the BBB
CEREBRAL METASTASIS
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CEREBRAL METASTASIS
Sources of Cerebral mets.in adults
Primary %
Lung CA 44%
breast 10%
kidney 7%
GI 6%
melanoma 3%
undetermined 10%
CEREBRAL METASTASIS
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Specific Types of Cerebral mets:
1.melanoma
-classically inv.the pia and arachnoid
-primary site cannot be identified in 14% of cases
2.Lung CA
-commonest source-radiosensitive
3.Renal Cell CA
Signs and symp.
-slowly progrssive
Evaluation:
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CT
-solitary in 50-65%
-arise in the gray-white matter junction
-profound white matter edema
-enhance
MRI
-more sensitive
Lumbar puncture
-useful in carcinomatous meningitis
Met.workup:
1.CXR
2.CT of the chest/abdomen
3.stool exam
4.mammogram
Management:
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-median survival=32 wks
-mostly palliative
Medical:
anticonvulsant
corticosteroid
H2 antagonist
Surgical mngt:
Solitary lesion
1.primary dse. Is quiescent
2.lesion accesible
3.symptomatic or life-threatening
4.dx.unknown
Multiple lesion
-irradiation
CEREBRAL METASTASIS
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Outcome:
resection of single mets+postop radiotx=8 months
Radiotx=15 wks
Steroids=2 months
Not tx=1 month