Tumors

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Tumors by Mind Map: Tumors

1. Ring enhancing lesions

1.1. GBM

1.2. Lymphoma

1.3. Mets

1.4. Resolving hematoma

1.5. Tumefactive MS

1.6. Astrocytoma

2. Geminoma

2.1. Sella/pineal region

2.2. Radiosensitive

3. Radiotherapy

3.1. SRS=SRS+WBRT SRS+WBRT=WBRT+Sgx SRS+WBRT>WBRT SRS>WBRT+Sgx (Level 3)

3.2. Schwanoma

3.2.1. SRS

3.2.1.1. 14 Gy

3.2.2. FSRT

3.2.2.1. 20-57.6 Gy

3.3. Clival tumors

3.3.1. 70 Gy

4. Sellar tumors

4.1. Craniopharyngioma

4.1.1. Aka Rathke's pouch or Hypophyseal duct tumors

4.1.1.1. But NOT Rathke's Cleft Cyst( !)

4.1.1.1.1. RCC are benign cystic remnants of the CRANIOPHARYNGEAL duct located at the sellar or the supracellar region

4.1.2. Bimodal presentation up to 15 yr/from 50 yr

4.1.3. 95% supracellar component

4.1.3.1. Panhypopituitarism w hypothalamic disturbances and weight gain, dysthermia and DI

4.1.3.2. Complete resection if no thalamic or optic components are present

4.1.3.3. RT

4.1.3.3.1. AE: Cavernomas, vascular malformations, meningiomas and maligant optic gliomas

4.1.3.4. Hormone panel work-up

4.1.3.4.1. 1) AM cortisol, 2) 17-hydroxycortisone, 3) GH, 4) prolactin, 5) T4, 6) FSH 7) LH 8) estradiol or testoserone 9) urinary free cortisol

4.1.3.4.2. endocrine dysfunction occurs in 90% pat

4.1.4. Adamantinomatous

4.1.4.1. Children

4.1.4.1.1. 70% mutation of Beta-catenin

4.1.4.2. Calcifications

4.1.4.3. Remnant of craniopharyngeal duct b/w Rathke's pouch and stomodeum

4.1.4.4. Mucin producing cells w goblet cells/columnar epithelium

4.1.4.4.1. Wet-keratin

4.1.4.4.2. Piloid gliosis w Rosenthal fibers

4.1.4.4.3. Granulomatous inflammation w Giant cells

4.1.4.5. 10x more common than papillary CPs

4.1.5. Papillary

4.1.5.1. Older

4.1.5.1.1. V600E and BRAF

4.1.5.2. Lack calcifications, goblet cells or cilliated epithelium

4.1.5.3. Metaplasia of adenohypophysial cells in the pars tuberalis

4.1.5.3.1. Picket fence-like pallisades

4.1.5.4. More often located around 3rd ventricle

4.1.6. Squamous cells of the pituitary stalk - tuber cinereum

4.1.6.1. MC nonneuroepithelial intracerebral tumor

4.1.7. Approaches; Sellar (transphenoidal), Supracellar (subfrontal if prefixed, pteronial for postfixed)

4.2. Pituitary tumors

4.2.1. Typical/atypical, functional/nonfunctional

4.2.1.1. 30% nonfunctional

4.2.1.2. >50% microadenomas

4.2.1.2.1. Secretory

4.2.1.3. Gonadotrophic secret LH, FSH but is clinically silent and present as macroadenomas

4.2.1.4. 3rd-6th decade of life

4.2.1.4.1. Secretory present earlier

4.2.1.4.2. nonfunctional present later due to mass effect

4.2.2. adenoma/carcinoma

4.2.2.1. Prolactinoma

4.2.2.1.1. Dopamine

4.2.2.1.2. MC functional

4.2.2.1.3. PRL levels=size

4.2.3. ACTH/GH/TSH

4.2.3.1. Dexametasone-suppression test

4.2.3.1.1. Inferior petrosal sampling

4.2.4. Pituicytomas

4.2.4.1. Rare, low-grade

4.2.4.2. Posterior hypophysis/ neurohypophysis

4.2.5. Management

4.2.5.1. Asx microadenomas that do not enlarge: observation

4.2.5.2. Asx Macroadenomas: observation w visual field and serial imagning.

4.2.5.3. Prolactinomas: Dopamine agonist (bromocriptine and cabergoline)

4.2.5.4. Somatotrophs: octreotide (suppress hromone prduction and causes tumor to shrink)

4.2.5.5. Pituitart apoplexy: Sgx and steroid replacement

4.2.6. Dgx

4.2.6.1. Imaging

4.2.6.1.1. Delayed contrast enhancement + less enhancement than normal tissue

5. Maligant Gliomas

5.1. MC primary maligancy/3rd intracranial maligancy

5.2. M>F

5.3. Familal 6%

5.3.1. BF type1&2 and Li-fraumeni

5.4. HA, seizures, personality changes and focal neurological changes

5.5. MRI

5.5.1. Irregular, poorly marginated, Gd enhancing lesions on T1 with ring enhancement

5.5.1.1. 40% of anaplastic astrocytomas do not enhance

5.5.2. No diffusion restriction

5.5.2.1. Hypointense on DWI

5.5.3. Spectroscopy

5.5.3.1. Proliferation (ratio choline/N-acetylasparate) and necrosis (lactate) suggest higher grade lesions

5.6. Anaplastic gliomas WHO III

5.6.1. Astrocytomas

5.6.2. Oligodendrogliomas

5.6.2.1. Histo: Fried-egg

5.6.3. Oligoastrocytes

5.6.4. Sgx/Bx and RT or Chz

5.6.4.1. Except for anaplastic astrocytomas WHO III gliomas are often treated w RT or Chx

5.7. GBM WHO IV

5.7.1. 80% de novo

5.7.2. Pseudopalisades

5.7.3. Keles/Laurix suggest that removal of 60% vs 89% of lesion strongly correlates with survival and tumor progress. UCSF suggested ~80%

5.7.4. Adjuvant therapy

5.7.4.1. FRT

5.7.4.1.1. 1.8 Gy x33

5.7.4.2. Chz

5.7.4.2.1. TMZ

5.7.4.2.2. Procarbazine, Lomustine and Vincristine

5.7.4.3. 2nd line therapy

5.7.4.3.1. Anti-vascular endothelial growth factor (anti-VEGF) and Bevacizumab

5.7.4.4. Molecular markers

5.7.4.4.1. metyhlated MGMT

5.7.4.4.2. 1p19q codeletion confers improved prognosis

5.7.4.4.3. IDH1 (astrocytomas) and IDH2 (oligodendrogliomas) mutation

5.7.4.4.4. Lack of amplification of EGFR/EGFRvIII

6. Nerve sheath tumors

6.1. Schwannomas

6.1.1. Essentic growth encapsulated within epinerium capsule

6.1.2. CNVIII and entry zone spinal senory

6.1.3. GTR and SRS

6.2. Neuromas

6.2.1. Not true neoplasm - inflammatory nidus consisting of Schwann cells, fibroblast and axons.

6.2.2. Rubbery and painful

6.3. Neurofibromas

6.3.1. Unencaspulated fusiform benign neoplasm that require nerve transection for complete removal

6.3.2. Not painful

6.4. Maligant peripheral nerve sheath tumors

6.4.1. Painful

6.4.2. NF1 50%

6.4.3. Resection and radiation

7. Germ cell tumors

7.1. Location pineal gland, neurohypophysis and basal ganglia

7.2. Germinoma

7.2.1. Two-cell pattern and cobblestone arrangement of large tumor cells with interstitial inflammatory cells

7.2.2. Upward gaze can be affected by compression of the tectum

7.2.3. CT detecting calcification, which may suggest a teratoma component

7.2.4. Radiation sensitive

7.2.5. Bifocal or synchronous tumors at neurohypophysis and pineal gland are pathognomonic

7.2.6. hCG positive

7.3. Nongerminomatous Germ Cell Tumors

7.3.1. Embryonal carcinoma

7.3.1.1. Pluripotent cells with inability to become germ cells.

7.3.1.2. Very maligant

7.3.1.3. positivity for cytokeratin, CD30, LIN28A, Oct4, and placental alkaline phosphatase (PLAP)

7.3.2. Yolk sac tumors

7.3.2.1. Endoermal sinus tumor

7.3.2.2. Schiller–Duval bodies glomeruli-like

7.3.2.3. AFP positive

7.3.3. Choriocarcinoma

7.3.3.1. Syncytiotrophoblasts and cytotrophoblasts

7.3.3.2. Intratumoral hemorrhage

7.3.3.3. Positive to β-hCG, cytokeratin, and EMA.

7.3.3.4. Hemorrhage: choricocarcinoma

7.3.4. Teratoma

7.3.4.1. Tissue derived from two or three germ layers (ectoderm, mesoderm, and endoderm), i.e. skin,bone etc.

7.3.4.2. Maligant degeneration into squamous cell carcinomas, adenocarcinomas, and rhabdomyosarcomas

7.3.5. Mixed germ cell tumors

8. Glial tumors

8.1. Grade I

8.1.1. Pilocytic astrocytomas

8.1.2. Subependymal giant cell astrocytoma

8.1.3. Subependymoma

8.2. Glioneuronal tumors

8.2.1. Pleomorphic xanthoastrocytoma

8.2.1.1. Children-Adolescents

8.2.1.2. Seizures

8.2.1.3. Superficial cortex, supratentorial, temporal lobe

8.2.1.4. Leptomeningeal

8.2.1.5. Cystic lesion and mural nodule

8.2.1.6. Calcifications are rare

8.2.1.7. Grade II, typically lack mitotic activity and lack of necrosis -> PXA anaplastic features Grade III

8.2.1.8. GTR

8.2.2. Dysembryoplastic Neuroepithelial Tumor

8.2.2.1. Children-Adolescents

8.2.2.2. Medically resistant seizures

8.2.2.2.1. Peritumoral cortical dysplasia

8.2.2.2.2. Post Sgx 80% improvement

8.2.2.3. Indolent and slow growing

8.2.2.3.1. Grade I

8.2.2.4. Temporal and frontal lobes

8.2.2.4.1. Cystic/bubbly

8.2.2.5. GTR

8.2.3. Ganglioglioma

8.2.3.1. MC temporal lobe EP

8.2.3.1.1. Can occur anywhere but 85% located in the temporal lobe

8.2.3.1.2. Partially cystic w nodule

8.2.3.2. M>F

8.2.3.3. Tendency to calcify

8.3. Cystic/bubbly

8.4. Grade II

8.4.1. Low grade astrocytoma

8.4.2. Mixed oligoastrocytoma

8.4.3. Presentation MC partial complex seizures, clinically undetected frequently

8.4.3.1. levetiracetam unlike phenytoin does not induce cytochrome P450 enzymes

8.4.4. growth 4.1 mm/y

8.4.5. Bx, Sgx, Chx, Rt

8.4.5.1. Bx 6% complication rate, 2% mortality rate and 8% failed bx

8.4.5.2. Intraoperative stimulation mapping: rolandic cortex, supplementary motor area, corona radiata, internal capsule and uncinate fascuculus

8.4.5.3. Awake language mapping: dominant hemisphere frontal operculum, temporal lobe or angular gyrus

8.5. Grade III

8.5.1. Anaplastic astrocytoma

8.5.1.1. Oligodenroglioma

8.5.1.1.1. Frontal lobes

8.5.1.1.2. Fried egg and chicken wire

8.5.1.1.3. Adults

8.5.1.1.4. Calcification

8.5.1.1.5. Anaplastic oligodendroglioma III vs Oligodenroglioma II

8.5.1.1.6. 1p19q deltion

8.5.1.1.7. IDH2

8.6. Grade IV

8.6.1. Glioblastoma multiforme

8.6.2. M>F

8.6.2.1. 60+

8.6.3. HA, seizures, personality changes and focal neurological

8.6.3.1. HA: early morning, asymmetrically, ipsilateral

8.6.4. Radiology: Irregular, poorly marginated, Gs enhanced on T1 hyperintense on T2

8.6.4.1. 40% of anaplastic astrocytomas lack enhancement

8.6.4.2. GBM typically have hemorrhage and necrosi

8.6.4.2.1. May be seen in corpus callosum and make it hard to diff from Lymphomas

8.6.4.3. DDx abscess have diffusion restriction on DWI and apperar hyperintense gliomas are hypointense

8.6.4.4. Spectroscopy: lactate (necrosis), ratio of choline to N-acetylaspartate (proliferation)

8.6.5. Pseudopalisades

8.6.6. Resection extent: Keles 60% of GD T1/T2, Lacroix 89% increases survial and 98% increased median survival 8.8 m to 13 m, USCF >78%

8.6.7. FRT 1,8 x33 =59.4 Gy w a margin of 2 cm beyond FLAIR bc local recurrence up to 80%

8.6.8. 1st line adjuvant therapy

8.6.8.1. 2nd line anti-VEGF and Bevacizumab

8.7. Prognosis oligodenroglioma>mixed astrocytomas>low grade astrocytoma (worse)

8.8. Molecular markers

8.8.1. P53

8.8.1.1. 1/3 of low grade diffuse astrocytomas

8.8.2. PTEN/FGFR

8.8.2.1. Upregulation seen in high-grade gliomas

8.8.3. 1p/19q deletion

8.8.3.1. Oligodenroglioma

8.8.3.2. PCV Chx and TMZ Chx

8.8.4. Methylation of MGMT

8.8.4.1. High grade

8.8.4.1.1. TMZ Chx

8.8.5. IDH1/2

8.8.5.1. Low grade gliomas

8.8.5.1.1. GBMs that have arisen from pre-existing low-grade tumors

8.8.5.1.2. IDH1 oligodendroglioma

8.8.5.1.3. IDH2 astrocytoma

8.8.6. Li fraumeni & NF1/2

8.8.7. Lack of EGFR mutation

8.8.7.1. Decreased proliferation capacity

8.9. UCSF prgnostic score

8.9.1. location of tumor in eloquent cortex

8.9.2. KPS <80

8.9.3. >50y

8.9.4. >4cm

8.9.5. >4 pt 56% 5-year survival

9. Mesenchymal tumors

9.1. Meningomas

9.1.1. arachnoid cap cells

9.1.1.1. F>M 2:1, cranial>spine 10:1 or 10% spinal, older age

9.1.1.2. arachnoid granulations along venous sinuses

9.1.2. Ionization radiation, NF2 chr 22

9.1.2.1. Progesterone receptors 50%

9.1.2.2. Multiple meningomas occur in 1-9% of sporadic cases and as a feature of NF2

9.1.2.3. 2-fold increased risk in F w breast Ca/BRCA1

9.1.2.4. SNPs, BRIP1/ATM

9.1.3. Grade I-III

9.1.3.1. Benign I

9.1.3.2. Atypical II

9.1.3.2.1. Mitoses >4/10hpf, small cell formation, prominent nuclei, sheetlike growth and areas of necrosis

9.1.3.3. Anaplastic III

9.1.3.3.1. Mitoses >20/10hpf, necrosis

9.1.4. Stain w positive EMA/Vimetin, negative s-100

9.1.4.1. DDx w Hemangioperiocytomas (metastasize 25-60%)

9.1.5. Grow 2-3 mm/y

9.1.6. Management

9.1.6.1. Observation if w/o parenchymal compromise and no neurovascular issues

9.1.6.1.1. Lack of T2 hyperintensity, peritumoral edema, calcification, irregular tumor borders and volumetric growth <1ml/yr

9.1.6.1.2. Symptomatic vs asymptomatic 4.3 vs 2.4 cm

9.1.6.2. Sgx

9.1.6.2.1. Simpsons grade

9.1.6.3. Chemo

9.1.6.3.1. Hormonal therapy w/o improvement in progression free survival (Mifepristone and Tamoxifen)

9.1.6.3.2. Hydroxyurea (arrest cell cycle and induce apoptosis)

9.1.6.3.3. Bevacizumab (antagonizes VEGF pathway)

10. Intraventricular tumors

10.1. Primary

10.1.1. Linning of ventricles

10.1.1.1. Ependymomas

10.1.1.1.1. NF2

10.1.1.1.2. Glial tumors w ependymal diff

10.1.1.1.3. 4th ventricle

10.1.1.1.4. Grade II

10.1.1.2. Subependymomas

10.1.1.2.1. Grade I

10.1.1.2.2. Glial tumors from subependymal layer attached to ventricular wall by a narrow pedicle

10.1.1.2.3. 4th ventricle >lateral ventricle

10.1.1.2.4. Incidental and can be managed conservatively

10.1.1.3. Colloid cysts

10.1.1.3.1. Bening 3rd ventricle epithelium lined cyst

10.1.1.3.2. Usually Asx ranging from few mm to 4cm, w resulting hydrocephalus and even sudden death

10.1.1.3.3. Filled w mucin, hemosiderin and cholesterol

10.1.1.4. Neurocytomas

10.1.1.4.1. Grade II

10.1.1.4.2. Rarely associated w sudden death

10.1.1.4.3. Foramen monro/3rd ventricle

10.1.1.4.4. histiologically appear very similar to oligodendrogliomas, salt-and-pepper apperance

10.1.1.4.5. Sgx currative

10.1.1.5. SEGAS

10.1.1.5.1. Not of astocystic origin

10.1.1.5.2. Almost exclusively associated w tuberous sclerosis

10.1.1.5.3. Asx unless large enough to cause hydrocephalus

10.1.1.5.4. MRI

10.1.1.5.5. mTOR inhibitors

10.1.2. Structures

10.1.2.1. Chorid plexus

10.1.2.1.1. Papillomas

10.1.2.1.2. Carcinomas

10.1.2.1.3. VHL

10.1.2.1.4. Hydrocephalus in 80% pat due to CSF overproduction

10.1.2.1.5. Commonly located supratentorially in children and infratentorially in adults

10.1.2.1.6. Angiography shows prominent blush w enlarged choroidal arteries

10.1.2.2. Meningomas

10.1.2.2.1. MC IV tumor, F>M, 4-6th decade, L>R side

10.1.2.2.2. Meningothelial inclusion bodies in the tela choroidea or the choroid plexus

10.2. Secondary

10.2.1. Craniopharyngiomas

10.2.2. Adenomas

10.2.3. Gliomas

10.3. Approaches

10.3.1. Transcallosal

10.3.1.1. works even w small ventricles

10.3.1.2. Short trajectory 3rd ventricle

10.3.1.2.1. no cortical transgressions

10.3.1.3. Con: weakness, akinetic mutism (cingulate gyrus) and memory deficist (fornices)

10.3.2. Endoscopic

10.3.2.1. dilation of ventricles is nedded

10.3.2.2. poor control in-case of bleeding

10.3.2.3. Pro: less invasive, direct vision, short postop time and less postop seizure

10.3.3. Transcortical-transventricular

10.3.3.1. right middle frontal gyrus

10.3.3.1.1. high risk for seizure

10.3.3.1.2. need for large ventricles

10.3.4. Subfrontal

10.3.4.1. Anterior-inferior 3rd ventricle

10.3.4.2. Subchiasmal, lamina terminalis

10.3.5. Stereotactic

10.3.5.1. enter just anterior to R coronal suture

10.3.5.2. endoscopic guidance

10.3.5.3. Good for cysts >1 cm viscous

11. Pineal region

11.1. Astrocytes, fibrovascular stroma and calcifications increasing w age

11.2. Pineal apoplexy

11.2.1. Diplopia, ocular motility, BS compression and endocrine

11.2.2. Parinaud syndrome

11.2.2.1. Upward gaze paralysis, lid retraction, light-near dissociation, unreactive pupils, convergence nystagmus, retraction nystagmus

11.3. Leptomeningeal disease

11.3.1. Germinomas, pineoblastomas, choricocarcinoma, pineal parenchymal tumor of intermediate differentiation

11.4. Serum markers

11.4.1. PIAP & Beta Hcg

11.4.1.1. Germinoma

11.4.2. AFP

11.4.2.1. Yolk sac

11.4.3. Beta Hcg

11.4.3.1. Mixed germ cell

11.5. Surgical aproaches

11.5.1. Dorsal midbrain and Vein of galen corridor must expand

11.5.1.1. Flat tentorium

11.5.1.1.1. Supracerebellar

11.5.1.2. step tentorium

11.5.1.2.1. Occipital transtentorial approach

11.6. Germinoma

11.6.1. Treated w radiation alone

11.7. Nongerminomatous Germ Cell Tumor (maligant NGGCT). Tx w platinum and spinal radiation

11.7.1. Image progression w/o markers suggest Growing teratoma syndrome (teratoma remnant after treatment of maligant gem cell component

11.7.2. Embryonal carcinoma, Teratoma, yolk sac, choricocarcinoma, mixed germ cell

11.8. Teratoma

11.8.1. Multicystic, may be part of NGGCT

11.8.2. Very resistant to chz or Rt

11.8.2.1. Sgx

11.9. Pineoblastoma

11.9.1. highly maligant

11.9.2. Chx and craniospinal RT

11.9.2.1. <3 yr no radiation

11.9.3. Trilateral retinoblastoma

11.10. Pineocytoma

11.10.1. low grade maligant

11.10.2. responds very well to surgical resection

11.11. Pineal parenchymal Tumor of Intermediate Differentiation

11.11.1. Intermediate maligance b/w pineoblastoma & pienocytoma

11.11.2. MIB-1 suggest more maligant

11.11.3. Tripple Tx

11.12. Papillary tumor of the Pineal region

11.12.1. Maligant tumors

11.12.2. GTR

11.13. Pineal cysts

11.13.1. Should be treated in children if Sx or growing

11.13.1.1. Grow during childhood

11.13.2. in adulthood the cyst may remain stable

11.13.2.1. can be followed if no Sx

11.13.3. Cyst >1-2 cm have greater tendency to be symptomatic

11.13.4. HA, hydrocephalus

11.13.5. Sudden headache may be due cyst apoplexy

11.13.5.1. Sgx

11.14. Rosette-forming Glioneuronal tumor of the pineal gland

11.14.1. Pineal gland or 4th ventricle

11.14.1.1. Responds very well to sgx, even subtotal

12. Acoustic Neuroma

12.1. Super division of VIII

12.1.1. sporadic

12.1.1.1. unilateral

12.1.1.2. 3rd-4th decade

12.1.2. NF2 5%

12.1.2.1. bilateral

12.1.2.2. younger

12.2. 8% of all intracranial tumors

12.3. Diagnosis

12.3.1. Asymmetric sensorineurnal hearing loss

12.3.1.1. predilection for higher freqency

12.3.1.2. Auditory Brainstem Response

12.3.1.2.1. delay in nerve conduction

12.3.1.2.2. upper limit of normal 0.2 ms

12.4. MRI GI enhanced

12.4.1. can detect 3-4 mm small lesions

12.4.2. Isointense T1 and T2

12.4.2.1. Homogenous enhancement on GI

12.5. Indications

12.5.1. Normal growth 0.6-3.4 mm/yr

12.5.2. Despite hearing loss w rapid tumor growth there is still excellent CNVII preservation rate

12.5.3. hearing preservation

12.5.3.1. >2.5 mm/yr

12.5.3.2. <2.5 mm/yr

12.5.3.3. Wait-and-see

12.5.3.3.1. 2.77-5.39 dB/yr hearing loss

12.6. Sgx

12.6.1. Middle fossa

12.6.1.1. better facial and hearing preservation as long as tumor <1.5 cm

12.6.2. Rectosigmoid

12.6.2.1. higher CNVII and hearing preservation for tumors >1.5 cm (or even >3 cm)

12.6.2.1.1. More postoperative HA and CSF leaks

12.6.3. Translabyrinthine

12.6.3.1. For pat with compromised hearing

12.6.3.1.1. Less HA and CSF leaks

12.6.4. Significant greater risk for V and VII funtional damage when comparing Sgx vs SRS

12.6.4.1. No diffrence in in tumor control vs SRS

12.7. SRS/LINAC

12.7.1. 12-14 Gy

12.7.2. High rate of tumor control & facial nerv function

12.7.2.1. lesions <3 cm

12.7.2.2. >90%-65%-98%

12.7.3. Hearing preservation 57-75%

12.8. Fractionated radiotherapy

12.8.1. Fractionated conventional RT

12.8.2. Fractionated stereotactic RT

12.8.2.1. More conformal radiation

12.8.2.2. 1.8-5 Gy

12.8.2.2.1. in total 20-57.6 Gy

12.8.2.3. Similar facial nerve function preservation and tumor control but mixed hearing preservation

12.8.2.3.1. lesions >3 cm

13. Posterior fossa tumors

13.1. most common

13.1.1. total metastasis

13.1.1.1. total 15% of all mets are in the cerebellum

13.1.1.2. 5% in the BS

13.1.1.3. Lung, breast, skin, kidney and colon

13.1.2. primary hemangioblastoma

13.1.2.1. 10% of primary posterior fossa

13.1.2.2. VHL chromosome 3

13.1.2.2.1. Retianl anc CNS hemangioblastoma

13.1.2.3. angio

13.1.2.3.1. vascular blush

13.1.2.3.2. fast filling and early washout

13.1.2.4. MRI

13.1.2.4.1. peritumoral cyst formation

13.1.2.5. Sgx with complete removal of the nodule

13.1.2.5.1. cyst wall removal is not needed

13.1.2.5.2. sgx is only needed when Sx

13.2. Cerebellar Pilocystic Astrocytoma

13.2.1. Survival is good

13.2.2. Cyst w contrast enhanced mural nodule

13.2.3. will lack the blush seen in the hemangioblastoma on angio

13.2.4. GTR

13.2.4.1. Cyst wall does not have to resected but Bx should ne taken

13.2.4.2. Radiation fo subtotal resection

13.3. 4th ventricle choroid plexus tumors

13.3.1. Rare in genral, even more so in adults

13.3.2. benign papilloma grade I, atypical grade II and carcinoma grade III

13.3.2.1. Heterogenous enhancement is suggestive of grade III

13.3.2.2. Sgx for lower grades and chz/RT for larger ones

13.3.2.3. Sgx for lower grades and chz/RT for larger ones

13.4. Brainstem glioma

13.4.1. adult gliomas are either low grade or high grade

13.4.1.1. low grade more common

13.4.1.2. Lesions are difffuse and surgical resection is hard

13.4.1.2.1. Radiation is primary treatment

13.4.1.3. High grade lesions enhance w contrast and exhibit areas of necrois and peritumoral edema

13.5. Medulloblastoma

13.5.1. Maligant

13.5.1.1. common in pediatric and rare in adults

13.5.2. midline verminan region

13.5.2.1. obstructive hydrocephalus

13.5.2.1.1. avoid shunting if possible as metastasis may occur

13.5.2.1.2. avoid shunting if possible as metastasis may occur

14. Clival tumors

14.1. Chordomas

14.1.1. slow-growing from the remnants of the primitive notochord

14.1.1.1. extradural clival tumors

14.1.1.1.1. spheno-occipital synchondrosis

14.1.1.2. skull base/spine>sacrum

14.1.2. histology

14.1.2.1. clear vaculoes and large septas

14.1.2.1.1. stains w brachyury, SOX-9 and podoplaning (to ddx from chondrosarcomas)

14.1.3. indolent tumors

14.1.3.1. diplopia and HA

14.1.3.1.1. cranial neuropathies and long tract signs

14.1.3.2. midline tumors w lytic bone destruction

14.2. Chondrosarcomas

14.2.1. orginate from cartilage producing mesenchymal cells

14.2.1.1. proximal long bones, pelvis, ribs and spine

14.2.1.2. clivus

14.2.1.2.1. majorityu are spontanous

14.2.1.2.2. may occur w Pagets, Olliers, Maffucci syndromes and Osteochondrosarcoma

14.2.1.2.3. Paramedially located unlike chondromas

14.2.1.3. diploia and HA

14.2.1.3.1. cranial neuropathies and long tract signs more common in chordomas

14.3. DDx: meningioma, paraganglioma, rhabdomyosarcoma, pituitary adenoma

14.4. Maxiumum surgical resection and high dose RT

15. Calvarial tumors

15.1. Benign

15.1.1. Epidermoid cyst

15.1.1.1. stratified sq cells

15.1.1.2. cyst filled with keratin

15.1.1.2.1. Dermoid cyst

15.1.1.3. Calvarial lesions in children at around ant fontanlele, coronal and lambdoid suture

15.1.1.4. Painless and slow growing

15.1.1.5. Surgical resection w cyst wall and avoidance of spillage that can cause severe chemical meningitis

15.1.2. Fibrous dysplasia

15.1.2.1. bone is replaced by fibrous tissue

15.1.2.2. usually begins w rapid bone growth in childhood and ceases in adulthood or puberty

15.1.2.3. sphenoid, frontal and maxillary bone

15.1.2.3.1. sclerotic, cystic or pagetoid

15.1.2.4. Symptomatic painful and deformity and optic nerve compromise

15.1.2.4.1. prophylatic optic decompression not indicated

15.1.3. Eosinophilic granuloma

15.1.3.1. Langerhans histiocytosis

15.1.3.1.1. epidermal dendritic cells

15.1.3.1.2. affect any organ

15.1.3.1.3. Hand-Schüller-Christian: DM, exophthalmos and lytic bone lesions usually involving the skull

15.1.3.1.4. Letterer-Siwe: Hepatomegaly, scaly skin lesions, lymphadenopathy and lytic bone lesions

15.1.3.2. M>F, frontal & parietal and painful lesions

15.1.3.3. Punched out lesions, destroy outer table>inner table

15.1.3.4. Sgx for single lesion and Chx/Rt for multiple lesion

15.1.4. Osteoma

15.1.4.1. Benign bone tumors

15.1.4.1.1. mature cortical bone

15.1.4.1.2. most common benign primary neoplasm

15.1.4.1.3. Multiple osteomas

15.1.4.1.4. Sinusitis due to sinus drainage

15.1.4.1.5. Surgery is indicated for symptomatic lesions

15.2. Maligant

15.2.1. Sarcoma

15.2.1.1. maligant tumors of mesenchymal tumors

15.2.1.1.1. Irregular, poorly marginated osteolytic lesions w/o adjacent sclerosis

15.2.1.1.2. Resection w wide margins and resection of infiltrated dura. Radiation/chx

15.2.2. Metastasis

15.2.2.1. Most common maligant tumor of the skull (adults and children)

15.2.2.1.1. Neuroblastoma

15.2.2.2. Growing skull lesion

15.2.2.2.1. neurovascular compression

15.3. Most common maligant tumor metastasis, osteoma most common primary benign and osteogenic sarcoma the most common maligant primary tumor

16. Paraganglioma

16.1. Imaging

16.2. Jugular formanen extension

16.2.1. Glomus jugulare (paraganglioma), schwannoma and meningioma

16.2.2. tumors that may invade the jugular foramen

16.2.2.1. chordoma, chondrosarcoma, endolymphatic sac tumor and metastases

16.3. other paragangliomas and pheochromocytoma

16.3.1. check urine catecholamine and urine vanillylmandelic acid levels

16.3.1.1. conversion of noepi to epi converted by PNMT present in the adrenal medulla

16.3.1.2. paragangliomas produce noepi

16.3.2. alpha and beta-blockade

16.4. very vascular lesions

16.4.1. preop embolization 3-5 days

16.4.2. generally the tumor pushes the lower cranial nerves (CN VII, IX, X, XI and CXII)

16.5. Treatment

16.5.1. RT

16.5.1.1. tumor control

16.5.1.1.1. no mortality and recurrence rate 2.1%

16.5.2. Sgx

16.5.2.1. 1.3% mortality and 3.1% recurrence rate