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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


3.2. Schwanoma

3.2.1. SRS 14 Gy

3.2.2. FSRT 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 But NOT Rathke's Cleft Cyst( !) 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 Panhypopituitarism w hypothalamic disturbances and weight gain, dysthermia and DI Complete resection if no thalamic or optic components are present RT AE: Cavernomas, vascular malformations, meningiomas and maligant optic gliomas Hormone panel work-up 1) AM cortisol, 2) 17-hydroxycortisone, 3) GH, 4) prolactin, 5) T4, 6) FSH 7) LH 8) estradiol or testoserone 9) urinary free cortisol endocrine dysfunction occurs in 90% pat

4.1.4. Adamantinomatous Children 70% mutation of Beta-catenin Calcifications Remnant of craniopharyngeal duct b/w Rathke's pouch and stomodeum Mucin producing cells w goblet cells/columnar epithelium Wet-keratin Piloid gliosis w Rosenthal fibers Granulomatous inflammation w Giant cells 10x more common than papillary CPs

4.1.5. Papillary Older V600E and BRAF Lack calcifications, goblet cells or cilliated epithelium Metaplasia of adenohypophysial cells in the pars tuberalis Picket fence-like pallisades More often located around 3rd ventricle

4.1.6. Squamous cells of the pituitary stalk - tuber cinereum 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 30% nonfunctional >50% microadenomas Secretory Gonadotrophic secret LH, FSH but is clinically silent and present as macroadenomas 3rd-6th decade of life Secretory present earlier nonfunctional present later due to mass effect

4.2.2. adenoma/carcinoma Prolactinoma Dopamine MC functional PRL levels=size

4.2.3. ACTH/GH/TSH Dexametasone-suppression test Inferior petrosal sampling

4.2.4. Pituicytomas Rare, low-grade Posterior hypophysis/ neurohypophysis

4.2.5. Management Asx microadenomas that do not enlarge: observation Asx Macroadenomas: observation w visual field and serial imagning. Prolactinomas: Dopamine agonist (bromocriptine and cabergoline) Somatotrophs: octreotide (suppress hromone prduction and causes tumor to shrink) Pituitart apoplexy: Sgx and steroid replacement

4.2.6. Dgx Imaging 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 40% of anaplastic astrocytomas do not enhance

5.5.2. No diffusion restriction Hypointense on DWI

5.5.3. Spectroscopy 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 Histo: Fried-egg

5.6.3. Oligoastrocytes

5.6.4. Sgx/Bx and RT or Chz Except for anaplastic astrocytomas WHO III gliomas are often treated w RT or Chx


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 FRT 1.8 Gy x33 Chz TMZ Procarbazine, Lomustine and Vincristine 2nd line therapy Anti-vascular endothelial growth factor (anti-VEGF) and Bevacizumab Molecular markers metyhlated MGMT 1p19q codeletion confers improved prognosis IDH1 (astrocytomas) and IDH2 (oligodendrogliomas) mutation 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 Pluripotent cells with inability to become germ cells. Very maligant positivity for cytokeratin, CD30, LIN28A, Oct4, and placental alkaline phosphatase (PLAP)

7.3.2. Yolk sac tumors Endoermal sinus tumor Schiller–Duval bodies glomeruli-like AFP positive

7.3.3. Choriocarcinoma Syncytiotrophoblasts and cytotrophoblasts Intratumoral hemorrhage Positive to β-hCG, cytokeratin, and EMA. Hemorrhage: choricocarcinoma

7.3.4. Teratoma Tissue derived from two or three germ layers (ectoderm, mesoderm, and endoderm), i.e. skin,bone etc. 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 Children-Adolescents Seizures Superficial cortex, supratentorial, temporal lobe Leptomeningeal Cystic lesion and mural nodule Calcifications are rare Grade II, typically lack mitotic activity and lack of necrosis -> PXA anaplastic features Grade III GTR

8.2.2. Dysembryoplastic Neuroepithelial Tumor Children-Adolescents Medically resistant seizures Peritumoral cortical dysplasia Post Sgx 80% improvement Indolent and slow growing Grade I Temporal and frontal lobes Cystic/bubbly GTR

8.2.3. Ganglioglioma MC temporal lobe EP Can occur anywhere but 85% located in the temporal lobe Partially cystic w nodule M>F 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 levetiracetam unlike phenytoin does not induce cytochrome P450 enzymes

8.4.4. growth 4.1 mm/y

8.4.5. Bx, Sgx, Chx, Rt Bx 6% complication rate, 2% mortality rate and 8% failed bx Intraoperative stimulation mapping: rolandic cortex, supplementary motor area, corona radiata, internal capsule and uncinate fascuculus Awake language mapping: dominant hemisphere frontal operculum, temporal lobe or angular gyrus

8.5. Grade III

8.5.1. Anaplastic astrocytoma Oligodenroglioma Frontal lobes Fried egg and chicken wire Adults Calcification Anaplastic oligodendroglioma III vs Oligodenroglioma II 1p19q deltion IDH2

8.6. Grade IV

8.6.1. Glioblastoma multiforme

8.6.2. M>F 60+

8.6.3. HA, seizures, personality changes and focal neurological HA: early morning, asymmetrically, ipsilateral

8.6.4. Radiology: Irregular, poorly marginated, Gs enhanced on T1 hyperintense on T2 40% of anaplastic astrocytomas lack enhancement GBM typically have hemorrhage and necrosi May be seen in corpus callosum and make it hard to diff from Lymphomas DDx abscess have diffusion restriction on DWI and apperar hyperintense gliomas are hypointense 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 2nd line anti-VEGF and Bevacizumab

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

8.8. Molecular markers

8.8.1. P53 1/3 of low grade diffuse astrocytomas

8.8.2. PTEN/FGFR Upregulation seen in high-grade gliomas

8.8.3. 1p/19q deletion Oligodenroglioma PCV Chx and TMZ Chx

8.8.4. Methylation of MGMT High grade TMZ Chx

8.8.5. IDH1/2 Low grade gliomas GBMs that have arisen from pre-existing low-grade tumors IDH1 oligodendroglioma IDH2 astrocytoma

8.8.6. Li fraumeni & NF1/2

8.8.7. Lack of EGFR mutation 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 F>M 2:1, cranial>spine 10:1 or 10% spinal, older age arachnoid granulations along venous sinuses

9.1.2. Ionization radiation, NF2 chr 22 Progesterone receptors 50% Multiple meningomas occur in 1-9% of sporadic cases and as a feature of NF2 2-fold increased risk in F w breast Ca/BRCA1 SNPs, BRIP1/ATM

9.1.3. Grade I-III Benign I Atypical II Mitoses >4/10hpf, small cell formation, prominent nuclei, sheetlike growth and areas of necrosis Anaplastic III Mitoses >20/10hpf, necrosis

9.1.4. Stain w positive EMA/Vimetin, negative s-100 DDx w Hemangioperiocytomas (metastasize 25-60%)

9.1.5. Grow 2-3 mm/y

9.1.6. Management Observation if w/o parenchymal compromise and no neurovascular issues Lack of T2 hyperintensity, peritumoral edema, calcification, irregular tumor borders and volumetric growth <1ml/yr Symptomatic vs asymptomatic 4.3 vs 2.4 cm Sgx Simpsons grade Chemo Hormonal therapy w/o improvement in progression free survival (Mifepristone and Tamoxifen) Hydroxyurea (arrest cell cycle and induce apoptosis) Bevacizumab (antagonizes VEGF pathway)

10. Intraventricular tumors

10.1. Primary

10.1.1. Linning of ventricles Ependymomas NF2 Glial tumors w ependymal diff 4th ventricle Grade II Subependymomas Grade I Glial tumors from subependymal layer attached to ventricular wall by a narrow pedicle 4th ventricle >lateral ventricle Incidental and can be managed conservatively Colloid cysts Bening 3rd ventricle epithelium lined cyst Usually Asx ranging from few mm to 4cm, w resulting hydrocephalus and even sudden death Filled w mucin, hemosiderin and cholesterol Neurocytomas Grade II Rarely associated w sudden death Foramen monro/3rd ventricle histiologically appear very similar to oligodendrogliomas, salt-and-pepper apperance Sgx currative SEGAS Not of astocystic origin Almost exclusively associated w tuberous sclerosis Asx unless large enough to cause hydrocephalus MRI mTOR inhibitors

10.1.2. Structures Chorid plexus Papillomas Carcinomas VHL Hydrocephalus in 80% pat due to CSF overproduction Commonly located supratentorially in children and infratentorially in adults Angiography shows prominent blush w enlarged choroidal arteries Meningomas MC IV tumor, F>M, 4-6th decade, L>R side 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 works even w small ventricles Short trajectory 3rd ventricle no cortical transgressions Con: weakness, akinetic mutism (cingulate gyrus) and memory deficist (fornices)

10.3.2. Endoscopic dilation of ventricles is nedded poor control in-case of bleeding Pro: less invasive, direct vision, short postop time and less postop seizure

10.3.3. Transcortical-transventricular right middle frontal gyrus high risk for seizure need for large ventricles

10.3.4. Subfrontal Anterior-inferior 3rd ventricle Subchiasmal, lamina terminalis

10.3.5. Stereotactic enter just anterior to R coronal suture endoscopic guidance 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 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 Germinoma

11.4.2. AFP Yolk sac

11.4.3. Beta Hcg Mixed germ cell

11.5. Surgical aproaches

11.5.1. Dorsal midbrain and Vein of galen corridor must expand Flat tentorium Supracerebellar step tentorium 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 Sgx

11.9. Pineoblastoma

11.9.1. highly maligant

11.9.2. Chx and craniospinal RT <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 Grow during childhood

11.13.2. in adulthood the cyst may remain stable 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 Sgx

11.14. Rosette-forming Glioneuronal tumor of the pineal gland

11.14.1. Pineal gland or 4th ventricle Responds very well to sgx, even subtotal

12. Acoustic Neuroma

12.1. Super division of VIII

12.1.1. sporadic unilateral 3rd-4th decade

12.1.2. NF2 5% bilateral younger

12.2. 8% of all intracranial tumors

12.3. Diagnosis

12.3.1. Asymmetric sensorineurnal hearing loss predilection for higher freqency Auditory Brainstem Response delay in nerve conduction 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 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 >2.5 mm/yr <2.5 mm/yr Wait-and-see 2.77-5.39 dB/yr hearing loss

12.6. Sgx

12.6.1. Middle fossa better facial and hearing preservation as long as tumor <1.5 cm

12.6.2. Rectosigmoid higher CNVII and hearing preservation for tumors >1.5 cm (or even >3 cm) More postoperative HA and CSF leaks

12.6.3. Translabyrinthine For pat with compromised hearing Less HA and CSF leaks

12.6.4. Significant greater risk for V and VII funtional damage when comparing Sgx vs SRS No diffrence in in tumor control vs SRS


12.7.1. 12-14 Gy

12.7.2. High rate of tumor control & facial nerv function lesions <3 cm >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 More conformal radiation 1.8-5 Gy in total 20-57.6 Gy Similar facial nerve function preservation and tumor control but mixed hearing preservation lesions >3 cm

13. Posterior fossa tumors

13.1. most common

13.1.1. total metastasis total 15% of all mets are in the cerebellum 5% in the BS Lung, breast, skin, kidney and colon

13.1.2. primary hemangioblastoma 10% of primary posterior fossa VHL chromosome 3 Retianl anc CNS hemangioblastoma angio vascular blush fast filling and early washout MRI peritumoral cyst formation Sgx with complete removal of the nodule cyst wall removal is not needed 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 Cyst wall does not have to resected but Bx should ne taken 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 Heterogenous enhancement is suggestive of grade III Sgx for lower grades and chz/RT for larger ones 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 low grade more common Lesions are difffuse and surgical resection is hard Radiation is primary treatment High grade lesions enhance w contrast and exhibit areas of necrois and peritumoral edema

13.5. Medulloblastoma

13.5.1. Maligant common in pediatric and rare in adults

13.5.2. midline verminan region obstructive hydrocephalus avoid shunting if possible as metastasis may occur 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 extradural clival tumors spheno-occipital synchondrosis skull base/spine>sacrum

14.1.2. histology clear vaculoes and large septas stains w brachyury, SOX-9 and podoplaning (to ddx from chondrosarcomas)

14.1.3. indolent tumors diplopia and HA cranial neuropathies and long tract signs midline tumors w lytic bone destruction

14.2. Chondrosarcomas

14.2.1. orginate from cartilage producing mesenchymal cells proximal long bones, pelvis, ribs and spine clivus majorityu are spontanous may occur w Pagets, Olliers, Maffucci syndromes and Osteochondrosarcoma Paramedially located unlike chondromas diploia and HA 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 stratified sq cells cyst filled with keratin Dermoid cyst Calvarial lesions in children at around ant fontanlele, coronal and lambdoid suture Painless and slow growing Surgical resection w cyst wall and avoidance of spillage that can cause severe chemical meningitis

15.1.2. Fibrous dysplasia bone is replaced by fibrous tissue usually begins w rapid bone growth in childhood and ceases in adulthood or puberty sphenoid, frontal and maxillary bone sclerotic, cystic or pagetoid Symptomatic painful and deformity and optic nerve compromise prophylatic optic decompression not indicated

15.1.3. Eosinophilic granuloma Langerhans histiocytosis epidermal dendritic cells affect any organ Hand-Schüller-Christian: DM, exophthalmos and lytic bone lesions usually involving the skull Letterer-Siwe: Hepatomegaly, scaly skin lesions, lymphadenopathy and lytic bone lesions M>F, frontal & parietal and painful lesions Punched out lesions, destroy outer table>inner table Sgx for single lesion and Chx/Rt for multiple lesion

15.1.4. Osteoma Benign bone tumors mature cortical bone most common benign primary neoplasm Multiple osteomas Sinusitis due to sinus drainage Surgery is indicated for symptomatic lesions

15.2. Maligant

15.2.1. Sarcoma maligant tumors of mesenchymal tumors Irregular, poorly marginated osteolytic lesions w/o adjacent sclerosis Resection w wide margins and resection of infiltrated dura. Radiation/chx

15.2.2. Metastasis Most common maligant tumor of the skull (adults and children) Neuroblastoma Growing skull lesion 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 chordoma, chondrosarcoma, endolymphatic sac tumor and metastases

16.3. other paragangliomas and pheochromocytoma

16.3.1. check urine catecholamine and urine vanillylmandelic acid levels conversion of noepi to epi converted by PNMT present in the adrenal medulla 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 tumor control no mortality and recurrence rate 2.1%

16.5.2. Sgx 1.3% mortality and 3.1% recurrence rate