Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
205 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What is the estimated annual incidence of primary CNS tumors in the U.S.?
|
~50,000 - 55,000 cases/yr of CNS tumors (per the National Program of Cancer Registries database)
|
|
|
|
What is the most common intracranial tumor?
|
Brain mets (~20-40% of all cancer patients develop brain mets)
|
|
|
|
What is the most common type of primary CNS tumor?
|
Glioma (~40%) > meningioma (15-20%)
|
|
|
|
What % of adult astrocytomas are low grade vs. high grade?
|
25% low grade vs. 75% high grade
|
|
|
|
What is the most common histological type of malignant CNS tumor in children? in adults?
|
Children: junvenile pilocytic astrocytoma (JPA) (20% <14 yo vs. 12% > 14 yo)
Adults: glioblastoma |
|
|
|
What is the strongest risk factor for developing CNS tumors?
|
ionizing RT in children (no threshhold - glioma, meningioma, nerve sheath)
|
|
|
|
What CNS tumors are linked to NF-1?
|
optic glioma, JPA
|
|
|
|
What CNS tumors are linked to NF-2?
|
bilateral acoustic neuroma, spinal ependymoma
|
|
|
|
What CNS tumors are linked to tuberous sclerosis?
|
subependymal giant cell astrocytoma, retinal hamartoma
|
|
|
|
What CNS tumors are linked to Von Hippel-Lindau?
|
hemangioblastoma
|
|
|
|
What CNS tumors are linked to Li-Fraumini?
|
glioma
|
|
|
|
What CNS tumors are linked to cowden syndrome (PTEN mutation)?
|
meningioma
|
|
|
|
What CNS tumors are linked to gorlin syndrome (basal cell nevus syndrome)?
|
medulloblastoma
|
|
|
|
What CNS tumors are linked to turcot syndrome (mismatch repair cancer syndrome, MMRCS)?
|
medulloblastoma; glioblastoma
|
|
|
|
What CNS tumors are linked to retinoblastoma?
|
pineoblastoma
|
|
|
|
What CNS tumors are linked to ataxia telangiectasia?
|
CNS lymphoma
|
|
|
|
What CNS tumors are linked to MEN I?
|
pituitary adenoma
|
|
|
|
What are the 4 factors used for grading in the WHO brain tumor grading system?
|
1. nuclear Atypia
2. cellularity and Mitosis 3. Endothelial proliferation 4. Necrosis (AMEN) |
|
|
|
What CNS tumors tend to have CSF spread?
|
- medulloblastomas and other blastomas (except astroblastoma/GBM)
- CNS lymphoma - choroid plexus carcinomas - germ cell tumors - mets. |
|
|
|
What CNS tumors have Flexner-Wintersteiner rosettes?
|
Pineoblastoma and RB (any PNET)
|
|
|
|
What CNS tumors have psamomma bodies?
|
meningioma and pituitary tumors (uncommon)
|
|
|
|
What CNS tumor type exhibits Verocay bodies?
|
Schwannomas
|
|
|
|
What CNS tumor type exhibits Schiller-Duval bodies?
|
yolk sac tumors
|
|
|
|
What receptors are commonly overexpressed in gliomas?
|
EGFR (30-50% GBM tumors) and PDGFR (non-GBM tumors)
|
|
|
|
neural stem cells express which marker? why are they important?
|
CD133. neural stem cells are thought to be precursors for astrocytomas
|
|
|
|
What gene on chromosome 17 is frequently lost in both high grade and low grade gliomas?
|
p53
|
|
|
|
What is the genetic mutation in NF-1, and for which sites does it predispose to gliomas?
|
In NF-1, the genetic mutation is 17q11.2/neurofibromin. It predisposes to optic/intracranial gliomas.
|
|
|
|
What brain region is associated with expressive aphasia?
|
the broca motor area (dominant/left frontal lobe) is associated with expressive aphasia
|
|
|
|
What brain region is associated with receptive aphasia?
|
the dominant/left temporal lobe at the posterior end of the lateral sulcus (wernicke area) is associated with receptive aphasia.
|
|
|
|
Which CN exits on the dorsal side of the midbrain?
|
CN IV (trochlear nerve) exits on the dorsal side of the midbrain
|
|
|
|
What structure produces CSF?
|
choroid plexus
|
|
|
|
What structures are in the cavernous sinus?
|
CNs III (occulomotor), IV (trochlear), VI (abducens), V1 (opthalmic branch of trigeminal), V2 (maxillary branch of trigeminal), and the internal carotid artery.
|
|
|
|
What is the cavernous sinus?
|
The cavernous sinus of each side is a venous space inside the skull through or next to which a number of important structures run. It is larger behind than in front and there is one on either side of the body of the sphenoid bone
|
|
|
|
What common defect does tumor involving the cavernous sinus produce?
|
CN VI palsy (abducens nerve palsy, eye does not move laterally; patient may see double vision when looking toward the side of the lesion)
|
|
|
|
What components traverse the superior orbital fissure?
|
CNs III (occulomotor), IV (trochlear), VI (abducens) and V1 (opthalmic branch of trigeminal)
|
|
|
|
What nerve passes through the foramen rotundum?
|
V2
|
|
|
|
What nerve passes through the foramen ovale?
|
V3
|
|
|
|
What structures pass through the foramen spinosum?
|
middle meningeal artery and vein, and nervus spinosus (branch of V3)
|
|
|
|
Through what structure do CNs VII-VIII traverse?
|
internal auditory meatus
|
|
|
|
Through which foramen does CN VII traverse the skull base?
|
stylomastoid foramen
|
|
|
|
most common type of intracranial tumor?
|
brain mets (~170,000/year)
|
|
|
|
what percentage of cancer patients develop brain mets?
|
20-40%
|
|
|
|
What is a "solitary" brain met?
|
one brain met; only site of disease
|
|
|
|
What is a "single" brain met?
|
one brain met in presence of extracranial disease
|
|
|
|
Which primary cancers are most likely to metastasize to the brain?
|
lung, breast, melanoma
|
|
|
|
Which primary cancers cause hemorrhagic mets?
|
renal cell, melanoma, and choriocarcinoma
|
|
|
|
Two scoring systems for determining prognosis?
|
1. RTOG recursive partitioning analysis (Gaspar, 1997)
2. Graded prognostic index (Sperduto 2008) |
|
|
|
RPA class I
|
KPS 70-100, primary tumor is controlled, age <65; median survival = 7.1 months
|
|
|
|
RPA class II
|
those not in class I or class III; median survival 4.2 months
|
|
|
|
RTOG RPA class III and IV for malignant glioma?
|
anaplastic astrocytoma, age 50 or less, abnormal MS, or age >50, symptoms < 3 months; GBM age <50 or age >50 and KPS 70 or above. Median survival?
|
11-18 months
|
|
|
What factors are used to determine graded prognostic index (Sperduto 2008)?
|
age, KPS, number of CNS mets, and presence of extracranial disease
|
|
|
|
A high (3.5-4.0) GPI score indicates what?
|
median survival of 11 months
|
|
|
|
Is there a role for steroids in asymptomatic patients?
|
no
|
|
|
|
steroids mainly improve what symptoms?
|
headache and neurologic function
|
|
|
|
Do steroids have an impact on survival?
|
no
|
|
|
|
How should we taper steroids?
|
as tolerated
|
|
|
|
We want to give steroids, what should we give?
|
start dexamethasone 4mg q6h
|
|
|
|
What are options for treating a single lesion; RPA class I-II?
|
- Surgical resection + WBRT (can also do SRS to tumor bed; contraversial)
- WBRT + SRS - SRS alone (with SRS or WBRT for salvage) - WBRT alone |
|
|
|
What are options for treating 2-4 lesions, RPA class I-II?
|
- WBRT alone
- WBRT + SRS - SRS alone (with SRS or WBRT for salvage therapy prn; contraversial) |
|
|
|
What are the options for treating >4 lesions; RPA class I-II?
|
- WBRT alone
- WBRT + SRS (contraversial) - SRS alone (with SRS or WBRT for salvage prn; contraversial) |
|
|
|
surgery + WBRT vs. WBRT alone in solitary brain lesions (Patchell 1990)
asking the question "do we need surgery at all or can we just give radiation?" |
- 54 patients with solitary brain lesion randomized to surgical removal of tumor + WBRT (36 Gy in 12 fxns) vs. needle biopsy + WBRT (same).
- Recurrence at original site, time to recurrence, MS, time to death from neuro cause, and time with KPS > or equal to 70 all significantly better in the surgery group. - Six pts excluded when resection or biopsy did not demonstrate pathologic diagnosis of brain met. |
|
|
|
surgery alone vs. surgery + WBRT in solitary brain lesions. (Patchell 1998). Asking the question "do we need radiation at all or can we just do surgery?"
|
- 95 patients with solitary brain lesions treated with surgery randomized to WBRT (50.4 Gy in 28 fxns) vs. no further therapy.
- Post-op RT reduced recurrence at original site and other sites in the brain. - Patients in RT group were less likely to die of neurological causes. - OS and duration of functional independence were not different. |
|
|
|
observation vs. WBRT after gross- total resection or SRS in patients with 1-3 brain mets (EORTC 22952-26001; Mueller 2009)
|
345 patients with WHO PS 0-2, 1-3 brain mets treated with resection (GTR) or SRS (20 Gy) randomized to observation vs. WBRT (30 Gy in 10 fxns).
- WBRT decreased 6, 24 months intracranial progression (15%, 31% vs. 40%, 54%) and neurologic death (25% vs. 43%). - no difference in OS or preservation of performance status. |
|
|
|
WBRT alone or with radiosensitizer efaproxiral? (Suh et al. 2006)
|
515 RPA class I-II pts with 1 or more brain mets randomized to WBRT alone (30 Gy in 10 fxns) vs. WBRT (same) + concurrent efaproxiral (increases oxygen carrying capacity of Hgb).
- 50% of pts had 3 or more mets - Trend of MS benefit of efaproxiral (4.4 vs. 5.4 months). - Largest improvement in breast cancer patients. |
|
|
|
WBRT alone or with radiosensitizer motexafin gadolinium (MGd)
|
- 554 pts with brain mets from NSCLC, KPS at least 70, randomized to WBRT alone (30 gy in 10 fxns) vs. WBRT (same) + concurrent MGd
- 80% of pts had more than one brain met. - Trend of improved time to neurologic progression with MGd (10 vs. 15 months) - Less salvage needed with MGd without change in MS (5.8 vs. 5.1 months) |
|
|
|
Maximum tolerated dose for single fraction radiosurgery?
|
tumor <20mm: 24 Gy
tumor 21-30mm: 18 Gy tumor 31-40mm: 15 Gy (Redmond generally does 18 (1-2cm), 16 (>2cm)?? i think) |
|
|
|
WBRT accepted fractionation schemes
|
4 Gy x 5 (20 Gy in 5 fxns)
- 3 Gy x 10 (30 Gy in 10 fxns; most common) - 2.5 Gy x 15 (37.5 Gy in 15 fxns) - 2 Gy x 20 (40 Gy in 4 weeks) |
|
|
|
WBRT techniques
|
- opposed laterals, flash ant/post/superior
- bottom of field at foramen magnum, inf to C1 or C2 (We go to below C2) - use eye block |
|
|
|
Follow up after WBRT or SRS to brain for mets?
|
MRI with and without contrast every 3 months.
|
|
|
|
Meninges are composed of what? (outer to inner)
|
dura matter --> arachnoid matter --> subarachnoid space. (PAD from inside out)
|
|
|
|
precentral gyrus
|
primary motor strip
|
|
|
|
postcentral gyrus
|
primary somatosensory cortex
|
|
|
|
medial aspect of pre and postcentral gyri relate to what part of the body
|
body, lower extremities, feet.
|
|
|
|
lateral aspect of pre and postcentral gyri relate to what part of the body
|
trunk, arms, and head
|
|
|
|
where is the Broca's (motor) area
|
dominant frontal lobe just superior to the lateral sulcus (sylvian fissure)
|
|
|
|
what is controlled by broca's area
|
it's the side of expressive aphasia. They can comprehend but are not fluent
|
|
|
|
where is wernicke's area and what is the significance?
|
dominant temporal lobe at posterior end of lateral sulcus; site of receptive aphasia (fluent but not able to comprehend)
|
|
|
|
what is the diencephalon?
|
thalamus, hypothalamus, and pineal gland.
|
|
|
|
what is the telencephalon?
|
olfactory lobes, cerebral hemispheres, basal gangli, and the amygdala.
|
|
|
|
what composes the mesencephalon (or midbrain)?
|
tectum, crus cerebri, superior and inferior colliculi, and cerebral aqueduct.
|
|
|
|
which cranial nerve exits from the dorsal surface of the midbrain?
|
CN IV
|
|
|
|
What is the course of CSF?
|
choroid plexus, lateral ventricles, foramen of Monroe, 3rd ventricle, cerebral aqueduct of sylvius, 4th ventricle, foramen of Magendie and two lateral foramen of lushka.
|
|
|
|
What is within the cavernous sinus?
|
CN III, IV, VI, and V1, V2 and the internal carotid artery.
|
|
|
|
involvement of the cavernous sinus commonly produces what?
|
CN VI palsy
|
|
|
|
Tumors with high propensity for CSF spread include?
|
medulloblastomas, primitive neuroectodermal tumors (PNETs), and CNS lymphoma.
|
|
|
|
Which tumors have a low propensity for CSF spread?
|
germ-cell tumors and ependymomas.
|
|
|
|
Which CNs exit the superior orbital fissure?
|
III, IV, VI and V1
|
|
|
|
which CN exits the foramen rotundum
|
V2
|
|
|
|
which CN exits the foramen ovale
|
V3
|
|
|
|
What goes through the foramen spinosum?
|
middle meningeal artery and vein
|
|
|
|
what goes through the internal auditory meatus?
|
CN VII, VIII
|
|
|
|
what goes through the jugular foramen?
|
CN IX, X, and XI
|
|
|
|
what goes through the hypoglossal canal?
|
CN XII
|
|
|
|
On a lateral plain film, where is the hypothalamus?
|
1 cm sup to sellar floor
|
|
|
|
on lateral plain film, where is the optic canal?
|
1 cm sup and 1cm anterior to the hypothalamus (which is 1 cm from sellar floor)
|
|
|
|
on lateral plain film, where is the pineal body (supratentorial notch)?
|
1cm posterior and 3 cm sup to external acoustic meatus
|
|
|
|
what covers the spinal cord and condenses into dentate ligaments?
|
pia matter
|
|
|
|
what does the arachnoid contain?
|
CSF (normal pressure 70-200 mmH2O lying down, 100-300mm standing up, total volume ~150mg)
|
|
|
|
where does the dura end?
|
S2
|
|
|
|
where does the cord end in adults?
|
L1, conus ends at L2.
|
|
|
|
where does the cord end in newborns?
|
~L3-4
|
|
|
|
incidence of malignant primary brain tumors?
|
2008 ~21,000. 13,000 deaths.
|
|
|
|
what percentage of primary cns tumors are malignant?
|
40%
|
|
|
|
incidence of adult primary CNS tumors?
|
30-35% meningioma, 20% GBM, 10% pituitary, 10% nerve sheath, 5% low grade glioma, <5% anaplastic astrocytoma, <5% primary CNS lymphoma.
|
|
|
|
what percentage of adult gliomas are high grade?
|
80%. 20% are low grade.
|
|
|
|
CNS tumors in kids. types and percentage?
|
20% of all peds tumors. 20% JPA, 15-20% malignant glioma/GBM, 15% medulloblastoma, 5-10% pituitary, 5-10% ependymoma, <5% optic nerve glioma.
|
|
|
|
possible etiologic associations of cns tumors?
|
rubber compounds, polyvinyl chloride, N- nitroso compounds, and polycyclic hydrocarbons.
|
|
|
|
Prior ionizing RT has been associated with what?
|
new meningiomas, gliomas, and sarcomas (~2% at 20 years)
|
|
|
|
NF-1 leads to what?
|
peripheral nerve sheath neurofibromas, cafe au lait spots, optic and intracranial gliomas, and bone abnormalities.
|
|
|
|
What's the deal with NF-1?
|
von Recklinghausen, chromosome 17q11.2, 1/3500 live births, NF-1 encodes neurofibromin, autosomal dominant, 50% germline, 50% new mutation
|
|
|
|
NF-2 leads to what?
|
bilateral acoustic neuromas, gliomas, ependymomas, and meningiomas
|
|
|
|
What's the deal with NF-2?
|
chromosome 22, 1/50K live births, NF-2 encodes merlin, autosomal dominant
|
|
|
|
what is von Hippel-Lindau disease
|
chromosome 3, AD, renal clear cell carcinoma, pheochromocytoma, hemangioblastoma, pancreatic tumors, and renal cysts
|
|
|
|
What's the deal with tuberous sclerosis? (Bourneville's disease)
|
TSC1 on chromosome 9, TSC2 on chromosome 16, AD, subependymal giant cell astrocytoma, retinal and rectal hamartomas.
|
|
|
|
retinoblastoma is due to mutation in what?
|
Rb tumor suppressor gene, chrom 13.
|
|
|
|
Turcot's syndrome is associated with what?
|
primary brain tumors with colorectal cancer
|
|
|
|
Li-fraumini syndrome is associated with what?
|
germline p53 mutation leading to breast, sarcoma, and brain CA
|
|
|
|
what is unique about genetics of neuroblastoma?
|
N-myc amplication commonly seen and serves as a prognostic factor.
|
|
|
|
FLAIR stands for...
|
fluid attenuation inversion recovery (it removes increased CSF signal on T2)
|
|
|
|
Tumor enhancement with gad correlates with...
|
breakdown of BBB
|
|
|
|
MRI of high grade vs. low grade
|
high grade usually has increased signal on T1 post and T2 (T2 also shows edema). Low grade has increased signal on flair
|
|
|
|
acute blood looks like what on MRI
|
increased signal on T1 pre-gadolinium
|
|
|
|
When should we get post-op MRI?
|
within 48 hours to document any residual disease after surgery
|
|
|
|
JPA on MRI?
|
enhancing nodule, highly vascular, 50% associated with cysts, high uptake on PET
|
|
|
|
Grade 2 glioma on MRI?
|
nonenhancing, hypodense on T1, hyperintense on T2/FLAIR, well-circumscribed, solid, round, calcifications associated with oligodendroglioma.
|
|
|
|
Grade 3 glioma on MRI?
|
enhancing with gad, infiltrative, less well-defined borders, mass effect (sulcal effacement, midline shift, ventricular dilation, and vasogenic edema).
|
|
|
|
GBM on MRI?
|
rim enhancing, central necrosis, irregular borders, and mass effect.
|
|
|
|
dural tail sign:
|
could represent tumor or increased vascularity, linear meningeal thickening and enhancement associated with some tumor adjacent to meninges, reported in 60% of meningioma, also seen in chloroma, lymphoma, and sarcoidosis.
|
|
|
|
n-acetylaspartate in MR spectroscopy
|
is a neuronal marker
|
|
|
|
choline (MR spect)
|
marker of cellularity and cellular integrity
|
|
|
|
creatine (MR spect)
|
marker of cellular energy
|
|
|
|
lactate (MR spect)
|
marker of anaerobic metabolism
|
|
|
|
characteristics of tumor on MR spectroscopy?
|
increased choline, decreased creatine, decreased NAA.
|
|
|
|
characteristics of necrosis on MR spect?
|
increased lactate, decreased choline, creatine, and NAA.
|
|
|
|
WHO grading system of gliomas?
|
Grade 1 = JPA, grade 2 = fibrillary astrocytoma, grade 3 = anaplastic astrocytoma, grade 4 = glioblastoma mutiforme
|
|
|
|
How are astrocytomas graded?
|
nuclear Atypia
Mitoses Endothelial proliferation Necrosis (AMEN) |
|
|
|
Pseudopalisading and necrosis?
|
GBM
|
|
|
|
Rosenthal fibers associated with what?
|
JPA (juvenile pilocytic astrocytoma)
|
|
|
|
psammoma bodies associated with what?
|
meningioma
|
|
|
|
verocay body is associated with what?
|
schwannoma
|
|
|
|
Schiller-duval body is associated with what?
|
yolk-sac tumor
|
|
|
|
Homer-wright rosettes are associated with what?
|
medulloblastoma, pineoblastoma
|
|
|
|
Flexner-Wintersteiner rosettes are associated with what?
|
pineoblastoma
|
|
|
|
benefit of 3D CRT over IMRT?
|
better dose homogeneity, fewer hot spots
|
|
|
|
GTV1 in high grade gliomas?
|
T1 enhancement +T2/FLAIR
|
|
|
|
CTV1 in high grade glioma?
|
GTV1 + 2 cm margin
|
|
|
|
Cone down: GTV2 and CTV2?
|
T1 enhancement only, and GTV2 + 2cm
|
|
|
|
Low grade gliomas: GTV?
|
tumors often nonenhancing, may be best visualized on FLAIR. GTV1=T1 enhancement or FLAIR for oligodendrogliomas.
|
|
|
|
Low grade gliomas: CTV?
|
GTV + 1-2 cm margin
|
|
|
|
Low grade gliomas: PTV?
|
CTV + 0.3-0.5 cm
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of whole brain?
|
50 Gy
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of partial brain?
|
60 Gy
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of brain stem?
|
54 Gy
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of spinal cord?
|
45 Gy
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of chiasm
|
50-54 Gy
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of retina
|
45
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of lens
|
10
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of inner ear
|
30 (with increasing risk of hearing deficit with increasing dose)
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of epilation (hair loss)
|
20-30
|
|
|
|
dose tolerance (using 1.8-2.0 gy/fx) of lacrimal gland
|
30 transient; 60 permanent
|
|
|
|
SRS max point dose for the brainstem
|
12
|
|
|
|
SRS max point dose for optic nerve and chiasm
|
8 Gy
|
|
|
|
SRS max point dose for visual pathway?
|
12 Gy
|
|
|
|
Fetal dose from cranial RT ?
|
0.05-0.1% of total dose (<0.1 Gy).
|
|
|
|
Acute RT complications in CNS?
|
alopecia, radiation dermatitis, fatigue, transient worsening of symptoms due to edema, nausea, and vomitting (particularly with brainstem (area postrema) and posterior fossa irradiation), and otitis externa. Mucositis, esophagitis, and myelosuppression are associated with cranopspinal irradiation.
|
|
|
|
acute reactions we typically think of subsiding within...
|
4-6 weeks after radiation
|
|
|
|
acute reactions are dose related or not?
|
dose related
|
|
|
|
Subacute reactions to CNS radiation?
|
somnolence, fatigue, neurologic deterioration, perhaps caused by changes in capillary permeability and transient demyelination.
|
|
|
|
Subacute reactions we typically think of being within...
|
6wks to 6 months after treatment
|
|
|
|
Late reactions to CNS radiation?
|
radiation necrosis, diffuse leukoencephalopathy (especially with chemo, but not necessarily correlated with clinical symptoms), hearing loss, retinopathy, cataract, visual changes, endocrine abnormalities, vasculopathy, moyamoya syndrome, decreased new learning ability, short term memory and problem solving skills
|
|
|
|
malignant gliomas are multicentric in what percentage of cases
|
5%
|
|
|
|
majority of malignant gliomas are...
|
glioblastoma
|
|
|
|
how do malignant gliomas present?
|
headache (50%), seizures (20%)
|
|
|
|
Prognostic factors used in RTOG RPA classes for malignant gliomas?
|
anaplastic astrocytoma vs. GBM
age 50 or less KPS > 70 mental status symptoms > 3 months |
|
|
|
survival benefit for the addition of temozolomide to RT seen in patients with what?
|
with MGMT promoter methylation.
|
|
|
|
RPA class I and II? median survival?
|
anaplastic astrocytoma, age 50 or less, normal mental status, or age >50, KPS >70, symptoms >3 months. MS is 40-60 months.(3-6 yrs)
|
|
|
|
RPA class III and IV? MS?
|
anaplastic astrocytoma, 50 or less, normal MS, or age >50, KPS >70, symptoms <3 months. glioblastoma age <50, or age >50 and KPS 70 or above. MS 11-18 months
|
|
|
|
RPA class V and VI?
|
glioblastoma, age >50, KPS <70 or abnormal mental status. MS 5-9 months.
|
|
|
|
general treatment recommendations for resectable or partially resectable malignant glioma
|
adjuvant RT to 60 Gy + concurrent temozolomide x 6 mo (6 monthly cycles) (stupp et al 2005 and 2009) OR 40 Gy/15 fxns for age 60 or above, and KPS >50 (Roa et al 2004) Or 30 Gy/10 fxns for age 65 or above and KPS <50 (Bauman).
|
|
|
|
dose for malignant glioma?
|
EBRT 1.8-2 Gy/fx to 45-46 Gy followed by cone down to 59.4 -60
|
|
|
|
follow up for malignant gliomas?
|
MRI 2-6 weeks after RT and then every 2 months
|
|
|
|
low grade gliomas are __ % of primary intracranial tumors
|
10%
|
|
|
|
oligodendrogliomas account for < ___% of intracranial tumros
|
<5%
|
|
|
|
age of onset for LGG?
|
30-40 for WHO grade II and 10-20 for JPA.
|
|
|
|
how do LGGs present?
|
seizures (60-70%, have a better prognosis) > HA > paresis
|
|
|
|
LGG favorable prognostic factors?
|
age <40, good KPS, oligo subtype, GTR, low proliferative indices, 1p/19q deletions for oligodendroglioma
|
|
|
|
Median survival for low grade and high grade gliomas?
|
pure oligodendroglioma (120 mo) > low-grade mixed oligogastrocytoma > low grade astrocytoma (60 mo) > or = anaplastic oligodendroglioma (60 mo) > anaplastic astrocytoma (36 mo) > GBM (12mo)
|
|
|
|
UCSF standard dose for LGGs?
|
1.8 Gy per fraction to 50.4-54 Gy
|
|
|
|
LGG GTV?
|
T1 enhancement or FLAIR
|
|
|
|
LGG CTV?
|
GTV +1-2cm margin
|
|
|
|
LGG PTV?
|
CTV +0.3-0.5cm
|
|
|
|
brain stem glioma is more common in young or old patients?
|
young
|
|
|
|
brain stem glioma accounts for __% of adult and __% of pediatric CNS tumors.
|
5%, 15%
|
|
|
|
incidence of brainstem gliomas peaks between ages ___ and ___
|
4 and 6
|
|
|
|
70-80% of brainstem gliomas are____. the rest are what?
|
high grade astrocytomas, remaining are low grade astrocytomas, ependymomas, PNETs, and atypical teratoid-rhabdoid tumors
|
|
|
|
astrocytoma is a subtype of a what?
|
glioma.
|
|
|
|
in brainstem glioma, what is sometimes not performed due to high morbidity and mortality?
|
biopsy
|
|
|
|
grade of brainstem glioma is determined by...
|
MRI and presentation
|
|
|
|
Describe high grade brain stem gliomas.
|
infiltrative, often originate in the pons, extend along white matter tracts into the cerebellum or diencephalon, diffusely expand the brainstem, younger age, rapid onset of symptoms, multiple neuro deficits.
|
|
|
|
Describe low grade brain stem gliomas
|
focal lesions in the midbrain or thalamus, or dorsally exophytic lesions, older age, and indolent course.
|
|
|
|
DDx of brain stem glioma (nondiffuse)?
|
abscess, neurofibromatosis, demyelinating diseases, AVM, encephalitis.
|
|
|
|
Brain stem glioma: 2-5 year OS in adults? kids?
|
45-66% in adults, 20-30% in kids.
|
|
|
|
Median survival for high grade brain stem gliomas?
|
11 months
|
|
|
|
Treatment recommendations for brain stem gliomas?
|
steroids
shunts (in severe hydrocephalus), surgery (role is limited) XRT (conventional fractionation to 54-60 Gy) chemo shows no benefit |
|
|
|
(**** not finished)brain stem gliomas: how do we treat them?
|
- conventional fractionation to 54-60 Gy
- for diffuse lesions cover the tumor with 2cm margin or entire brainstem (diecephalon to T2) |
|
