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Diagnostic imaging of Intracranial neoplasms Part I

Diagnostic imaging of Intracranial neoplasms Part I. Witold Gajewicz Department of Radiology Medical University of Lodz. Classification of intracranial neoplasms. There is no an ideal one Bailey and Cushing, Russel and Rubinstein, WHO, new WHO classification.

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Diagnostic imaging of Intracranial neoplasms Part I

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  1. Diagnostic imaging of Intracranial neoplasmsPart I Witold Gajewicz Department of Radiology Medical University of Lodz

  2. Classification of intracranial neoplasms There is no an ideal one Bailey and Cushing, Russel and Rubinstein, WHO, new WHO classification

  3. Classification of intracranial neoplasms One can make it by: Histology Primary Glial Non glial Metastatic Age and general location Adult primary brain tumors Primary brain tumors in children Specific anatomic location

  4. Classification of intracranial neoplasms Specific anatomic location Pineal region masses Intraventricular masses Cerebellopontine angle masses Foramen magnum masses Sellar/suprasellar masses Skull base and cavernous sinus masses Scalp, cranial vault, and menigeal masses

  5. Classification of intracranial neoplasms general location Intraaxial neoplasms Extraaxial neoplasms

  6. Glial neoplasms • incidence: 2/3 of brain neoplasms are primary tumors ½ of primary tumors are gliomas ¾ of gliomas are astrocytomas More than ¾ astrocytomas are anaplastic astro and GBMs In the whole group of gliomas: • 45 - 50% are GBMs • 20 - 25% anaplastic astrocytomas • 10 - 20% benign = low grade astrocytomas (fibrillary and pilocytic) • 5 - 10% oligodendrogliomas

  7. Low grade astrocytomas Age: children and young adults 20-40 y.o Location: brain hemispheres, subcortical Children: posterior fossa – pilocytic astrocytoma (1/3 of children gliomas) Natural history: 5 -10 years survival

  8. Low grade astrocytomas • Imaging: • Low density in CT • In MRI low signal intensity in T1w and high in T2w frequently cystic tumor • in cystic tumors like (astrocytoma pilocyticum, pleomorphic xanthoastrocytoma) there is an inhomogenous contrast enhancement of the small mural nodule and cyst wall

  9. pilocytic astrocytoma

  10. Low grade astrocytomas • imaging: • - In solid tumors WHO G1, G2 there is a lack or very weak contrast enhencement • In smaller low grade tumors G1, G2 the mass effect can be also only slightly visible

  11. Astrocytoma G2

  12. Astrocytoma G2

  13. Glioblastoma Age: Adults > 50 y.o, rarely < 30 y.o Location: cerebral hemispheres, mainly white matter Natural history: very rapid diffuse growth of tumor, less than 2 years of survival even after the succesfull surgery!

  14. Glioblastoma • Imaging: • Focal lesion of the mixed signal intensity on MR, and mixed density on CT examination • thick irregular „rind” of tissue around the necrotic center • inhomogenous structure • often bleeding • extensive peritumoral oedema FINGER TYPE OEDEMA! • strong inhomogenous enhancement

  15. Glioblastoma

  16. Glioblastoma PD w T2 w

  17. Glioblastoma T1 w T1 w gado

  18. Glioblastoma Tumors like GBM and anaplastic astrocytoma spread along: . White matter tracts . Subpial space . Subarachnoidal space and arachnoid . Ependyma and leptomeninges, rarely dural invasion and extracerebral metastases . GBM can be multifocal and metabolically is a disease of the whole brain, even the non affected hemisphere

  19. Common routes of spread of GBM and other anaplastic glial tumors

  20. Meningiomas Most frequent non glial neoplasm, 15-20% of primary brain tumors. 1 – 9% multifocal Age: 40 – 60 y.o., 2-4 x more in women Natural history: Depends on location and possibility of removal Metastases are rare but possible both from benign and malignant tumors

  21. Meningiomas • Characteristic locations: • olfactory groove • parasellar • sphenoid ridge • parasaggital • cerebral falx • cerebellar tentorium • temporal bone pyramid apex • temporal bone pyramid internal acoustic porus

  22. Meningiomas Imaging: plain skull radiographs • - Changes in bone shape and structure with hyperostosis, thickening and small, short pinlike „processes” outside the bone (effect of thetumor spread along the Haversian channels) • - Enlargement and better visible Pacchioni granulations • Enlargement of and better visible vascular bone pattern • pathologic intracranial calcifications • - Skull bones changes caused by high intracranial pressure

  23. Meningiomas • Imaging: • * on CT more-less homogenous, hyperdense, well delineated lesion • inhomogenous with calcifications • * On MR hypointense on T1w and hyperintense on T2w but not much, may be inhomogenous (calcifications) • slight to moderate oedema: in larger tumors, located near skull and in malignat types • strong usually inhomogenous contrast enhancement with the characteristic „dural tail sign”

  24. convexity And cerebral falx

  25. Meningiomadural tail sign

  26. Schwannoma • Age: Adults, women 50 – 60 y.o, • Multiple, bilateral acustic nerve schwannomas -NF II - age 30 y.o • Location: • typical infratentorial – V, VII, VIII cranial nerves • - ponto-cerebellar angle tumor • internal acoustic meatus widening

  27. Schwannoma • homogenous tumor with the density CT and signal MR similar to brain tissue, larger ones are inhomogenous (bleeding, cysts, hyalination, calcifications) • characteristic image of an „ice cream on the cone” – tumor comes out of the widened int acoustic meatus = „cone” and forms a mass in the ponto-cerebellar angle „ice cream” • usually strong homogenous CE, sometimes inhomogenous

  28. Schwannoma ice cream on the cone sign

  29. Pituitary adenomas • microadenomas • up to 10 mm • intrasellar inside the gland • not spreadind outside the gland • not rising or crossing sellar diaphragm • isointense with the gland on T1w • in the initial phase of CE stay • hypointense the gland on CE T1w

  30. Pituitary adenomas microadenomas T1w CE T1w

  31. Pituitary adenomas – intrasellar tumors • macroadenomas • tumors spreading outside the gland and sella • may infiltrate sorrounding structures • homogenous CE • sometimes cystic • sometimes bleeding

  32. Pituitary adenomas macroadenomas on CT diagnosis is possible on MR precise evaluation of a local spread (cavernous sinus spread!)

  33. metastases • Location: • brain, • skull bones, • meninges, • subarachnoidal – usually multiple • Wiek: rare in children, more common over 40 y.o

  34. metastases • on CT iso or hypodense • on MR mixed signal depends on necrosis and bleeding • usually large zone of oedema on CT and MR • meta can be ring like or cystic because of necrosis • most commonly multiple • little meta may be invisible on CT or/and MR, especially without contrast administration

  35. metastases • bleeding is common especially in metastases from: lungs, breast and melanoma • strong to moderate CE both on CT and MR sometimes enables the correct diagnosis

  36. Metastases

  37. Metastases

  38. Cerebral vasculatureSTROKE (clinical definition) • sudden focal neurological deficit of persumed vascular origin which lasts more than 24 hours

  39. Cerebral vasculatureSTROKE • cerebral ischaemia • cerebral hemorrhage • venous thrombosis

  40. STROKE - etiologies • Cerebral infarction 80% • Large arteries: ICA, MCA, PCA 40-50% • small arteries – lacunar infarctions 25% • Cardiac emboli 15% • Blood disorders 5% • Nonatheromatuos occlusions (vasculitis, vasculopathy) 5%

  41. STROKE - etiologies • Primary intracranial hemorrhage 15% • Hypertension bleeds 40-60% • Amyloid angiopathy 15-25% • Vascular malformations 10–15% • Drugs (antykoagulants, sympathomimetics) 1-2% • Bleeding diathesis eg. thrombocytopenia<1%

  42. STROKE - etiologies • Nontraumatic subarachnoid hemorrhage 5% • aneurysm 75 - 80% • AVM 10 - 15% • Nonaneurysmal SAH 5 – 15% • Other 1% • Cerebral vein thrombosis and occlusion • Saggital sinus thrombosis and occlusion

  43. Cerebral stroke -CT What’s the question? Diagnose or exclude hemorrhage Identify the presence of an uderlying pathology: Tumor Metastasis AVM Subdural hematoma (1-2% of clinical stroke syndrom signs come from nonvascular disorders!)

  44. Cerebral infarctionpenumbra • In the most common situation due to MCA occlusion there is a densly ischaemic central focus area where cells are irreversibly damaged and a less densly ichaemic penumbra – in this area cells may be saved when the reperfusion is quickly established, but are at risk for several hours

  45. Cerebral infarction CT signs • up to 12 h (hyperacute) • normal 50-60% • Hyperdense artery 25-50% • obscuration of lentiform nuclei

  46. Cerebral infarction CT signs • Acute 12 - 24 h • Low density basal ganglia • Loss of GM - WM interfaces (insular ribbon sign) • Sulcal effacement • mass effect can appear

  47. Cerebral infarctionCT signs Insular ribbon sign Hyperdense MCA

  48. Cerebral infarction CT signs – subacute - after 24h • Wedge shaped hypodense area in both WM & GM • increasing mass effect • Haemorrhagic transformation from injured capillaries • Gyral enhancement - luxury perfusion • Mass effect • Oedema • later CE (from blood-brain barrier breakdown)

  49. Cerebral infarctionCT signs

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