brain mets ppt file.pptx7uuiikkkli9opmnnnnn

R

1. BRAIN METASTASIS MODERATOR :DR.RAMAKANTH ASSISTANT PROFESSOR PRESENTOR:DR.PRANAVI

2. Metastases are secondary tumors that arise from primary neoplasms at another site CNS metastases can arise from both extra and intracranial primary tumors . Metastases from extracranial primary neoplasms ("body-to-brain metastases") most commonly spread via hematogeneous dissemination. Direct geographic extension from a lesion in an adjacent Structure.

3. Invasion usually proceeds along paths of least resistance , i.e., through natural foramina and fissures where bone is thin or absent . Perineural and perivascular spread are less common but important direct geographic routes by which head and neck tumors gain access to the CNS. Primary intracranial neoplasms sometimes spread from one CNS site to another, causing brain-to-brain or brain-to-spine metastases.. Spread occurs preferentially along compact white matter tracts such as the corpus callosum and internal capsule but can also involve the ventricular ependyma , pia, and perivascular spaces.

4. CSF dissemination with " carcinomatous meningitis " and "drop metastases " to the brain and spine occurs with both extra- and intracranial primary neoplasms. Children : The most common sources of cranial metastases in children are hematologic malignancies. In descending order of frequency, they are leukemia, lymphoma, and sarcoma( osteogenicsarcoma , rhabdomyosarcoma, and Ewingsarcoma ). The preferential locations are the skull and dura . Parenchymal metastases are much less common in children compared with adults.

5. Adults. Metastases from lung, breast, and melanoma account for at least two-thirds of all brain metastases in adults. The overall most is lung cancer (especially adeno carcinoma and small cell carcinoma). Breast cancer is the second most common primary tumor source.

6. Skull, dura, and spine metastases are typically caused by prostate, breast, or lung cancer , followed by hematologic malignancies and renal cancers. Melanoma, renal cell carcinoma, and choriocarcinoma are especially prone to develop intratumoral hemorrhages .

7. PARENCHYMAL METASTASIS The brain parenchyma is the most common site(80%), followed by the skull and dura (15%). Diffuse leptomeningeal ( pial ) and subarachnoid space infiltration is relatively uncommon, accounting for just 5% of all cases. Only 15% of metastases are found in the cerebellum. The midbrain, pons, and medulla are uncommon sites (especially for solitary lesions) and account for less than 5% of metastases. Small cell lung carcinoma is the most common tumor that causes such " pseudogliomatous " infiltration.

8. NECT . iso - to slightly hypodense relative to gray matter .Sometimes, edema is the most striking manifestation of metastases on NECT. In the absence of edema or intratumoral hemorrhage, even moderately large metastases may be virtually invisible on NECT scans. With the exception of treated metastases, calcification is rare. CECT. majority of parenchymal metastases enhance strongly T1WI . Most metastases are iso - to mildly hypointense on T1WI The exception is melanoma metastasis , which has intrinsic T1 shortening and thus appears moderately hyperintense

9. T2/FLAIR . Many metastases appear hypointense on T2WI and FLAIR Multiple small hyperintense metastases ("military metastases") can be mistaken for small vessel vascular disease unless contrast is administered Both subacutehemorrhage and melanin cause prominent signal intensity loss ("blooming") on T2* (GRE, SWI) images T1 C+. Virtually all nonhemorrhagic metastases enhance following contrast administration .Patterns vary from solid, uniform enhancement to nodular,"cyst + nodule," and ring-like lesions. Multiple metastases in the same patient may exhibit different patterns

10. DWI:adenocarcinoma metastases tend to be hypointense small and large cell neuroendocrine carcinomas are hyperintense on DWI MRS Choline is generally elevated , and Cr is depressed or absent in most metastases Prominent lipid signal is the dominating peak on MRS inthe majority of brain metastases Early results using new agents such as F18-DOPA show promise in detecting disease relapse after surgical treatment

11. Skull/Dural Metastases Skull/Dural Metastases . Calvarial and skull base metastases can be relatively well circumscribed or diffusely destructive , Dural metastases usually occur in combination with adjacent skull lesions, appearing as focal nodules or more diffuse, plaque-like sheets of tumor Dural metastasis without skull involvement is much less common. Most dural metastases also involve the subjacent arachnoid and are actually dura-arachnoid tumor deposits

12. NECT. Large dural metastases buckling the gray-white matter interface CT circumscribed intraosseous lesions> Permeative , diffuselyde structive lesions osseous metastases— prostate ant breast cancer —can be blastic and sclerotic CECT. The most common finding is a focal soft tissue mass centered on the diploic space. A biconvex shape with bothsubgaleal and dural extension is typical enhance strongly Angiography: DSA is rarely used unless a vascular lesion is suspected. Mostmetastases —especially those from renal cell carcinoma—are hypervascular

13. T1WI. .Metastases replace hyperintense yellow marrow and appearas hypointense infiltrating foci in diploic space. FLAIR hyperintensity in the underlying sulci suggests pia subarachnoid tumor spread. Most dural metastases enhance strongly , appearing asbiconvex masses centered along the adjacent diploic space. Dural "tails" . Duralthickening can be smooth and diffuse or nodular and masslike .

14. Leptomeningeal Metastases Leptomeningeal Metastases . The term "leptomeningeal metastases"actually describes metastases to the subarachnoid spaces and pia. Diffuse opacification of the leptomeninges with sugar-like coating of the pia is typical. Multiple nodular deposits and infiltration of the perivascular (Virchow-Robin) spaces with extension into the adjacent cortexmay occur Rarely, metastatic tumor spreads under the pia ( subpialspread ).

15. contrast to dura-arachnoid metastases that "hug" theinner table of the calvaria , LM follow the brain surfaces , curving along gyri and dipping into the sulci. contrast- enhancedscans is as though the CSF "turns white CT Findings :Subtle sulcal-cisternal effacement with nearly isodense infiltrates can bes een replacing the hypodense CSF in some cases. MR Findings . T1 scans may be normal or show only smudged "dirty" CSF. Most LMs are hyperintense on T2WI and may be indistinguishable from normal CSF. FLAIR imaging shows loss of CSF suppression

16. CSF Metastases Both extra- and intracranial metastases can seed the CSF. Intracranial CSF metastases are usually seen as "dirty" CSF on T1WI and FLAIR, often occurring together with diffuse pial spread. “ "Drop metastases" into the spinal subarachnoid space are a manifestation of generalized CSF spread Ependymal spread around the ventricular walls occurs with primary CNS tumors much more often than with extracranial sources

17. PERINEURAL METASTASIS Pmost common nerves to be affected by PNT are the maxillary division of the trigeminal nerve ( CN V₂) and the facial nerve SCCa or melanoma of the cheek can infiltrate the infraorbital division of CN V₂. Posterior spread into the PTPF allows access to the cavernous sinus and Meckel cave via the foramen rotundum The mandibular nerve (CN V₃) can be invaded by any masticator space malignancy. Parotid gland malignancies such as adenoid cystic carcinoma can "creep" up the facial nerve all the way into the internal auditory canal

18. 1.Tubular enlargement of the affected nervetogether with widening of its bony canal or foramen is typical 2.If the nerve passes through a structure such as the PTPF that is normally filled with fat, the fat becomes "dirty" or effaced. 3.Look for denervation atrophy—common with CN V₃ lesions—seen as small, shrunken muscles of mastication with fatty infiltration. 4.If tumor extends into the cavernous sinus, the walls may bulge outward, and Meckel cave may be filled with soft tissue instead of CSF

19. MR Findings. The natural contrast provided by fat on T1WI is extremely helpful in detecting possible PNT. Obliterated fat—especially in the PTPF—is a key finding. PNT is often isointense with nerve and difficult to see on T2WI. Tumor spread into Meckel cave replaces the normal hyperintense CSF with isointense soft tissue. Postcontrast T1 scans should be performed with fatsaturation to increase conspicuity of the enlarged, strongly and uniformly enhancing nerve

20. Ventricles/Choroid Plexus Metastases The lateral ventricle choroid plexus is the most common followed by the third ventricle Solitary >multiple enlarge the choroid plexus Iso to hyperdense compared with normal choroid plexus on NECT scans. often hypervascular , so hemorrhage is quite common Most nonhemorrhagic choroid plexus metastases are hypointense to brain on T1WI and hyperintense on T2/FLAIR. Intense enhancement following contrast administration is typical. Choroid plexus metastases display a prolonged vascular "blush" on DSA.

21. Pituitary Gland/Infundibular Stalk Metastases A sellar mass with or without bone erosion, stalk thickening, loss of posterior pituitary "bright spot," and cavernous sinus invasion is typical but nonspecific. An infiltrating, enhancing pituitary and/or stalk mass is the most common finding

22. Ocular Metastases uveal tract -choroid m/c Breast cancer >lung ca mass that often enhances strongly after contrast administration

23. Direct Geographic Spread From Head and Neck Neoplasms CT scans show a solid mass with irregular margins and bone destruction. Sinonasal SCCa is isointense with mucosa on T1WI and mildly to moderately hypointense on T2WI. SCCa shows mild to moderate enhancement following contrast administration but enhances to a lesser extent than adenocarcinoma, esthesioneuroblastoma , and melanoma. Coronal T1 C+ FS images are recommended to delineate extension through the cribriform plate into the anterior cranial fossae

24. Thank you