Lytic leisons of the skull

Lytic leisons of the skull

1. LYTIC LESIONS OF THE SKULL

2. Lytic lesions of the skull have a wide range of different etiologies, ranging from normal variants to congenital, traumatic, inflammatory and neoplastic lesions, benign ones being more frequent than primary malignancies. Some of them are incidental findings in imaging studies, while many others manifest as palpable masses, with or without associated pain. Their true etiology may be puzzling considering their imaging features alone. Therefore, clinical information including the age of the patient, main diseases and previous physical trauma, including surgeries, is essential for the Radiologist to narrow the differential diagnosis.

3. Imaging approach frequently begins with radiographic and ultrasound studies, quite limited in most cases, CT and MR being complementary and the methods of choice, for the assessment of bone and associated soft tissue masses, respectively. MR is also able to depict bone marrow involvement, especially helpful at early stages. Conventional angiography may be useful for both, diagnosis and treatment.

4. Approach Detection Solitary or multiple Age- elderly/older adult or child/younger adult Well defined or ill defined Specific characteristics

5. 1. Detection X ray: including skeletal survey in some cases: evaluated as lytic or sclerotic CT: NECT/CECT: confirm nature of lesion (i.e., lytic or sclerotic), destruction in inner or outer table, calcification, sclerotic margins, and density MRI: For further characterisation of lesion. Bone scan

6. 2. Solitary or Multiple Solitary common Soiitary rare Multiple common Multiple rare Norma l variant Osteoporosis circumscripta Normal variant Hyperparathyroidism Surgical defect Epidermoid Surgical defect Myeloma Trauma Cephalocele Metastasis Osteomyelitis Dermoid Intradiploic arachnoid cyst Osteoporosis Eosinophilic granuloma Intradiploic meningioma Metastasis Leptomeningeal cyst Hemangioma

7. Older adult/ elderly  Metastasis/malignancy - breast, lung, melanoma, thyroid, RCC Multiple myeloma epidermoid / dermoid H aemangioma Intraosseous meningioma Hem angiopericytoma GCT Brown tumour Paget disease O steomyelitis normal variants : arachnoid granulation venous lake emissary vein parietal thinning surgical defect e.g. burr-hole  Child/ young adult Eosinophilic granuloma / histiocytosis E pidermoid / dermoid Fibrous dysplasia Hemangioma M etastasis Neuroblastoma Medulloblastoma Leukemia Growing skull fracture Meningocele Osteomyelitis normal variants : arachnoid granulation venous lake emissary vein F ontanelle Prominent convolutional markings surgical defect 3. Age

8. Metabolic

9. In general population, seven diagnosis include 85% of all causes - by decreasing order, dermo / epidermic cysts, hemangioma , metastasis, multiple myeloma, Langherans histiocytosis , Paget disease of bone and fibrous dysplasia. In adults, tumoral causes are predominant - metastasis and myeloma , whereas in children, besides congenital defects, dermoid cysts and eosinophilic granuloma are the most frequent diagnosis.

10. Normal Variants Osteolytic skull lesions may have many different causes, anatomical variations being responsible for up to 60% of cases.

11. Transcalvarial Venous Channels and Venous Lakes Consist of apertures in the skull through which emissary veins pass, connecting the venous sinuses of the dura mater with veins external to the skull. Look like serpiginous or linear lucencies with sclerotic borders through the skull, and are, therefore, occasionally mistaken for sutures or fractures. Enlarged veins within the diploic space are known as venous lakes , corresponding to round or oval lucent foci, frequently along the inner table of the skull. These normal structures show an intense enhancement after intravenous contrast administration on both, CT and MR.

12. Fig: Typical transcalvarial venous channels and venous lakes appearing on nonenhanced CT (a) as linear lucencies through the skull with sclerotic edge and round/ oval radiolucent foci with integrity of the outer calvarial table, respectively. These structures intensely enhance after gadolinium administration, as demonstrated on this T1-weighted MR image (b), which also shows a large falx meningioma .

13. Arachnoid Granulations also known as Pacchionian granulations. are normal anatomical structures visible in approximately 1% of patients corresponding to enlarged arachnoid villi that are involved in the filtration of CSF from the subarachnoid space to the venous system. Hypertrophic arachnoid granulations as a result of high CSF pressure may be responsible for lytic skull lesions. Most are located close to the superior sagittal sinus. Appear as rounded and sharply circumscribed lucencies with sclerotic border, seen on MR as projections within the sinus of signal intensity similar to that of CSF and on MR angiography as filling defects

14. Fig: Arachnoid granulation incidentally found in these non-enhanced CT scan (a) and T2-weighted MR (b) image, as a parasagital sharply circumscribed osteolytic lesion, remodelling inner calvarial table, isointense to CSF, which remained stable over time.

15. Enlarged Parietal Foramina autosomal dominant inherited condition. represent a benign variant of incomplete ossification of parietal bones , which are supposed to close during fetal development, by the fifth month of pregnancy. imaging appearance consists of circular and symmetrical openings on both sides of the sagittal suture with variable size, up to several centimetres wide. Although not usually associated with any medical problems, local pressure is painful and these patients being at higher risk of brain damage by local trauma. to avoid misinterpretation as pathological entities, it should always be reported.

16. Fig: Enlarged parietal foramina. Note the bilateral and almost symmetric rounded parietal calvarial defect, with smooth and sharp margins and without any associated soft tissue or vascular malformation. The 3D reconstruction (b) provides a particularly clear visualization of this variant.

17. Prominent Convolutional Markings Related to pulsation of brain Inner table, frequent in children Become prominent in craniosynostosis , chronic raised intracranial pressure

18. Treatment related

19. Congenital

20. Cephalocele Skull defect with herniated intracranial contents. Meningocele CSF lined by meninges Gliocele CSF lined by glial tissue Meningoencephalocele CSF and brain Meningoencephalocystocele CSF, brain and ventricles Atretic cephalocele Small nodule of fibrous-fatty tissue, dura and dysplastic brain tissue.

21. Encephaloceles , occasionally misdiagnosed as dermoid cysts. protrusion of cerebral and/or meningeal tissue through a congenital defect of the skull and dura , usually located at or near the midline with an associated palpable mass. In some cases, the skin and dura overlying the malformation is incompletely formed resulting in direct exposure of the arachnoid layer. Diagnosis is usually made antenatally by means of ultrasound, MR providing assessment of the contents of the herniated sac and subsequent risk of infection. The round cranial defect with sclerotic margins may be well demonstrated on radiographs and CT.

22. Fig: Encephalocele . T2-weighted sagittal MR images of a child presenting a small fluctuating mass over the posterior sagittal suture since birth, clearly depicts the herniation of the meninges and the brain tissue through a small bone defect.

23. Sinus Pericranii Abnormal communication between the intracranial and extracranial venous drainages, usually congenital. manifesting as a fluctuating mass in the scalp, which varies in size according to intracranial pressure changes. Ultrasound evaluation provides an accurate diagnosis . However, contrast-enhanced CT is a more popular method, showing an enhancing epicranial mass composed of serpiginous vessels. Although complication by thrombosis has been described, treatment has basically been recommended for aesthetic reasons. Preoperative endovascular embolization is a promising technique on preventing haemorrhage .

24. Fig: Sinus pericranii . Contrast-enhanced CT scan showed an epicranian lesion grossly in the midline, composed of multiple serpiginous venous structures. Sinus pericranii . (a) Lateral X ray: diffuse & more discrete areas of cortical thinning.

25. Fig. 8: The T1-weighted MR sagittal image (a) and the MR angiography (b) of the same patient clearly demonstrate the intracranial communication between the scalp venous malformation and the superior sagittal sinus, consistent with sinus pericranii .

26. Dermoid cyst Well-circumscribed unilocular cyst containing fat Expands diploe Location is key Commonly near the anterior fontanelle , glabella, nasion , vertex, subocciput tend to be midline in frontotemporal , parietal Most involve course of suture line near anterior fontanelle

27. Epidermoid cyst 20–50 years Mostly in parietal and temporal bones Intradiploic Well-defined with dense sclerotic margins Typically round or lobulated Contains cholesterol and keratin; d/t lipid content  hypoattenuating

28. Fibrous dysplasia Congenital disorder  expanding lesions with mixture of fibrous tissue and woven bone Defect in osteoblastic differentiation and maturation Monostotic (70%), polyostotic (25%), craniofacial (CFD) and syndromic Plain films: blistering/bubbling cystic skull vault lesion, commonly crosses suture, sclerotic skull base, obliteration of the paranasal sinuses. Radiolucent expansile area in diploe with thinning of the adjacent tables, mainly outer margins sharply defined and can be sclerotic- difficult to differentiate from epidermoid " Ground-glass " matrix in a bone lesion on CT Bone expansion, “ Ground glass ”

29. If cystic may have thick sclerotic "rind ” TlWI: low SI T2WI: low signal (if solid) or high SI (if "cystic") High SI if increase in clinical-pathologic activity Tl C+: Variable enhancement depends on lesion pattern (rim, diffuse, or none) CT or MRI to define local extent Bone scan to search for additional lesions & stage lucent cavity (arrow) and a thick sclerotic rind surrounded by a thin lucent rim "Ground glass" appearance on PF or CT and homogeneously decreased signal on T2WI characteristic

30. TRAUMATIC

31. Posttraumatic defect Skull defects may be posttraumatic, either surgical or as a result of high-energy trauma. Accurately evaluated by CT, usually require surgical repair.

32. Fig: Posttraumatic frontal bone defect as a result of severe trauma in a young woman CT scan (a). 3D reconstruction (b) provides an exquisite anatomic detail of the bone defect.

33. Leptomeningeal Cyst A late posttraumatic complication of 1% of skull fractures occurring under 3 years old, usually in parietal region. Late complication of skull fracture with dural laceration Exposure of the inner table of the skull to the CSF and arachnoid pulsations subsequent to a dural tear, result in herniation of CSF or brain parenchyma into the subcutaneous tissue. seen on both CT and MRI as a smoothly marginated skull defect with an associated cystic lesion. Lucent skull lesion with rounded scalloped margin and bevelled edges is typical.

34. Fig. 10: Leptomeningeal cyst. CT scan (a) of a 26 year-old man presenting with seizures, showed a small defect with bevelled edges in the right parietal bone with resultant mild deformity in the overlying scalp. MRI (b) demonstrated a cystic lesion insinuating into the eroded inner table, corresponding to the dilated overlying subarachnoid space.

35. 2 different forms: growing fractures & intradiploic arachnoid cysts Dural tear & herniation of CSF or brain parenchyma into sc tissue Growing fracture: widening of fracture line >4 mm ; involves both inner & outer tables Intradiploic arachnoid cysts: erode inner table rather than outer table. Diagnosis of a leptomeningeal cyst: history of trauma, bone defect, presence of gliosis in neighboring parenchyma, and the presence of cystic lesions having a CSF characteristic 63-year-old male; history of trauma in childhood; erosion of inner table of left parietal bone; bone defect into which herniation of brain parenchyma & CSF.

36. Others

37. Eosinophilic Granuloma A localized form of Langerhans cell histiocytosis . A systemic disease of unknown etiology, in which abnormal proliferation of histiocytes occurs, forming focal or diffuse clusters. Almost exclusively affects children and young adults, who present with a palpable mass, in the parietal area in most cases. characterized by a well-defined lytic lesion without marginal sclerosis, invading the inner and outer tables, sometimes with a central residual bone density within it, known as "button sequestrum “. Its MRI signal intensity is equivalent to that of skeletal muscle, with marked enhancement after intravenous paramagnetic contrast medium administration

38. X RAY: Best diagnostic clue: Sharply marginated lytic skull defect with beveled margins, lack of marginal sclerosis ± Button sequestra or sclerotic margins when h ealing

39. button sequestrum : L ytic lesion with intact central nidus of bone Bone replaced by erosive accumulation of histiocytes  lucent; central opacity represents an island of dead bone peripheral sclerosis : not seen unless the lesion is in the healing period; also may be seen in: metastatic carcinoma necrosis following radiotherapy epidermoid cysts calvarial tuberculosis Classification: multiple organ systems, multiple sites: Letterer- Siwe ds (10%) single-organ system, multiple sites: Hand- Schuller -Christian dis (20%) single lesion : eosinophilic granuloma (70%)

40. Calvaria: mostly frontal, parietal, then temporal mastoid Mastoid: Geographic destruction, often bilateral  middle ear bone deafness Mandible: “ floating tooth ” Greater wing of sphenoid  Orbital wall involve  proptosis

41. Fig. 11: Eosinophilic granuloma . CT scan of a 31 year-old woman presenting with a painful swelling in the midline scalp, revealed a sharply marginated lytic bone defect with bevelled margins.

42. Fig: Within the bone defect depicted in the patient of figure above, there was a soft tissue mass, which was better evaluated by means of MR, appearing heterogeneously hyperintense on T2 (a) and gadolinium-enhancing on T1-weighted images (b). Note the mild mass effect on the adjacent dura and gyri , without invasion.

43. Hemangioma Hemangioma is the main cause of primary bone tumours at the skull. Accounts for 10% of cases, middle-aged women being the most affected. Sharply marginated expansile skull lesion. Most are single, but may be multiple in 15% of cases. Although frequently asymptomatic, may manifest as a palpable mass. Diploic space; more often frontal & temporal. X ray: Sharply marginated expansile lesion May have thin peripheral sclerotic rim Honeycomb/ sunburst/ spoke wheel/ reticulated appearance

44. CT typically shows a well-defined lucent lesion with sclerotic margins and a reticulated internal structure radiating from the center to the periphery described as "sunburst" or "spoke-wheel" pattern. MRI better depicts the extension of the lesion and its relationship to the adjacent neurovascular structures. MRI: d/o fatty or vascular nature of hemangioma T1: low (vascular)/high (fatty) T2: high (vascular)/intermediate (fatty) T1C+: enhancement It is a strongly enhancing lesion on both, CT and MRI, after intravenous contrast medium administration.

45. Fig. 13: Hemangioma of the skull. The slow-growing left parietal scalp swelling of a 31 year-old woman consists of an expansile lytic lesion on radiograph (a), well circumscribed, with sclerotic margins and with the typical "sunburst" pattern of bony striations on non-enhanced CT scan (b).

46. Fig. 14: MRI of the same patient as in figure above provided good visualization of the compression of the brain by the bone lesion, which showed heterogeneous T2 (a) hyperintensity and intense enhancement after gadolinium administration on T1- weighted images (b). There is no surrounding edema.

47. fig. circular radiolucent defect present primarily within the temporal bone, with minimal extension into the frontal bone. There is an intense, radiating spiculation of bone from the central portion of the lytic defect, creating the  sunburst  or  spoked -wheel appearance of an intraosseous hemangioma

48. NECT: excellent characterization of trabecular & cortical detail Sharply marginated expansile lesion Thin peripheral sclerotic rim in 1/ 3 Intact inner & outer table Outer table often more expanded than inner table May deform overlying soft tissues " Spoke-wheel", "reticulated", or " weblike " pattern Intradiploic trabecular thickening " Soap bubble" & "honeycomb" appearance CECT : Enhances Fig. Surgical specimen X ray: sharply marginated expansile hemangioma with "soap bubble" appearance

49. Fig: Another calvarial hemangioma in young women presenting with frontal scalp swelling

50. Hemangiopericytoma Intracranial hemangiopericytoma , arise in pericytes that originate in the meninges . account for 1% of all central nervous system tumours . With a location similar to that of meningioma , usually occurs at an earlier age, are more aggressive, tend to recur and may metastize extracranially . Imaging studies demonstrate bone erosion and a narrow dural attachment in most of these heterogeneously enhancing lesions. unlike meningioma , is not associated with calcifications. Prominent internal flow voids on T2-weighted MR images is a typical feature. Preoperative embolization is recommended in order to reduce intraoperative haemorrhage .

51. Fig: Hemangiopericytoma . Coronal bone window (a) of a 4 year-old girl presenting with a marked focal scalp swelling in the midline of the parietal region, showed a soft tissue mass with bone destruction without peripheral sclerosis. Note the lobulated contour, the typical narrow base of dural attachment and the heterogeneous intense enhancement on T1-weighted MR images after gadolinium administration, which in association with the invasion of the skull, helped distinguish from a meningioma .

52. Fig. 18: The hypervascularization of the same hemangiopericytoma is also evident by the numerous intratumoral flow voids on T2-weighted MR images (a) and on the MR angiography (b).

53. Fig: The same lesion as in figures above evident on conventional angiogram by the tumor blush, supplied by the left superficial temporal, median meningeal and occipital arteries. Successful preoperative embolization verified on the control angiogram (b).

54. Meningioma : Osteolytic but usu sclerotic margins Predominantly after 30 yrs age Can result in: compression of adjacent brain parenchyma encasement of arteries compression of dural venous sinuses

55. Aneurysmal Bone Cyst Aneurysmal bone cysts may occur in any bone, but rarely in the skull, accounting for only 3-6% of all cases. Most are benign but may be locally aggressive. Present as painless, progressively rapidly-growing lesion in childhood and young adulthood Characteristic imaging appearance consists of an expanding osteolytic lesion containing blood-filled spaces of variable size, frequently with multiple small fluid-fluid levels representing sedimentation of red blood cells. Total excision is the treatment of choice, preoperative endovascular embolization significantly decreasing intraoperative bleeding.

56. Fig. 20: Aneurysmatic bone cyst in a 54 year-old women presenting with long-standing headache. Non-enhanced CT scan (a) demonstrated a large destructive mass in the left parietal bone, grossly lenticular with expansion of both, but predominantly the inner table of skull, with local mass effect. T2-weighted MR images (b) showed hyperintensity , consistent with its cystic nature, as well as some septations .

57. Fig.: T1 (a) hyperintensity of the same lesion . After gadolinium administration (b) the typical peripheral enhancement and the "soap-bubble" pattern, corresponding to multiple cystic cavities, are evident.

58. Fig: Effective preoperative embolization of the aneurysmatic bone cyst described above.

59. Multiple Myeloma A malignant bone marrow disorder characterized by monoclonal proliferation of plasma cells. Responsible for most primary bone lesions in advanced ages. The solitary form is designated by plasmacytoma . Typically appear as well-defined multiple, discrete, small, punched out lytic lesions without marginal sclerosis ‘ rain-drop ’ lesions  coalesce to form larger lesions lytic lesions, resembling punch holes. “ pepper pot skull ” Rarely sclerotic except following therapy

60. Enhance after intravenous contrast media administration, hypointense and hyperintense , respectively on T1 and T2-weighted MR images. NECT: Punched out lytic lesion; cortex is eroded from within sharply defined margins Best imaging tool : Radiography ( skeletal survey better than bone scan : osteolysis without bony reaction ) CT > MRI for evaluation of specific lesion extent MRI best for rare meningeal & " intracranial "

61. Fig: Uncountable lytic "punched out" lesions on the lateral skull radiograph, typical of multiple myeloma.

62. Fig: Myeloma lytic skull lesions on non-enhanced CT scan (a) of the same patient . MRI accurately depicts myelomatous infiltration with replacement of normal bone marrow as demonstrated in this T1-weighted images after gadolinium administration, showing anomalous enhancement with multiple lesions, which had a permeative pattern and T2 hyperintensity .

63. Multiple myeloma metastasis Sclerotic margins Very rare (2%) common Mandible involvement May be seen Rare Soft tissue extension Advanced cases Rare Pedicles and posterior elements are involved less frequently and at later stage than in mets

64. Metastasis to skull: 15-25% cancer pts Best diagnostic clue: Enhancing lesion(s) with skull/ meningeal destruction /infiltration Usu. multiple and osteolytic Lack sclerotic borders adults: lung, breast, prostate, melanoma, follicular thyroid children: neuroblastomas and sarcomas prostate ca : usu. sclerotic or mixed type, lateral orbital wall a favourite site thyroid & renal cell cancer: sclerotic and solitary In the presence of a known primary tumor, associated parenchymal metastases, and multiple lytic lesions, calvarium metastases be considered M ost instances, skeletal metastases represent advanced disease with poor prognosis. Metastatic neuroblastoma showing generalized moth-eaten destruction of calvarium, producing somewhat of a salt and pepper appearance.

65. X ray: Focal lytic or blastic lesions lacking " benign " sclerotic border CT: Enhancing mass centered in bone with osseous destruction , lacking 'benign" sclerotic border MR: T1WI low, T2WI high T1C+: Lesion may enhance to "normal" T1 marrow signal ~ Fat saturation necessary to distinguish enhancement from normal hyperintense marrow & scalp fat

66. Fig. 26: Skull metastasis. Multiple expansile osteolytic lesions in a patient with long-standing rectal carcinoma. MRI features are usually similar to those of multiple myeloma lesions, namely the T2 hyperintensity (a) and the heterogeneous enhancement on T1-weighted images after gadolinium administration (b).

67. Paget ’ s disease Chronic, excessive bone remodeling Lytic Phase : early phase osteolysis , unopposed osteoclastic activity well-defined, often large areas of radiolucency most commonly frontal and occipital bones osteoporosis circumscripta both tables notable absence of peripheral sclerosis surrounding the calvarial osteolysis secondary to the lack of significant osteoblastic activity. Mixed Phase: osteoblastic + clastic vast majority , active stage “ mosaic pattern ” Sclerotic/ blastic / Burn-out Phase: dense pagetic bone Lytic phase of Paget disease of the skull with osteoporosis circumscripta . (a) Lateral radiograph of a 50-year-old man shows a well-defined area of lysis in the frontal and occipital regions (arrowheads).

68. X ray: Large, round, lucent area in the left parietal bone CT: lytic abnormality involving the left parietal bone that was well differentiated from normal-appearing calvarial bone Bone scan: marked uptake in the calvaria Osteoporosis circumscripta 87F with raised Alkaline phosphatase - Kirsten M. Leu, NEJM 2002

69. Fig. multiple lucent lesions of the skull representing brown tumors , as well as generalized "salt and pepper" demineralization of the calvarium ; patchy area of sclerotic repair bone in the frontal region. Hyperparathyroidism: osteitis fibrosa cystica: classic skeletal manifestation of advanced hyperparathyroidism osteoclastic resorption of bone, osteoblastic bone formation, and fibrous replacement of marrow most common radiologic is osteopenia , Subperiosteal bone resorption is early and virtually pathognomonic sign areas of decreased radiopacity are intermingled with sclerotic radiopaque areas  classic appearance “ salt-and-pepper ” skull

70. Hyperparathyroidism with "salt and pepper" appearance of the calvarium from generalized spotty demineralization. Multiple well-defined lytic lesions represent brown tumors

71. Leukemia with widespread lytic lesions of the calvarium Leukemia

72. Sarcoidosis : May be multiple or solitary With or without bone expansion Erosion or areas of destruction of inner and/or outer tables Extension intracranially or into extracranial soft tissues Can have ci rcumscribed and/or indistinct margins Differential considerations : Hemangioma eosinophilic granuloma metastases other tumors as well as chronic infection

73. Osteomyelitis Usually complication of trauma, sinusitis, mastoiditis Frontal > temporal bone Mixed lytic /proliferative lesion Moth-eaten/ permeative medullary & cortical destruction - patchy bone destruction " Pott puffy tumor" = frontal soft tissue swelling Often associated: Epidural abscess ! i.e. bone destruction, soft tissue swelling & abscess Osteomyelitis in sickle cell disease. Several foci of osteomyelitis, with somewhat serpiginous radiolucent areas of destruction surrounded by minimal sclerotic borders, are noted in the frontal and parietal bones of this child.

74. Lipoma: expansile lytic lesions with well-defined margins may have sclerotic borders may show central calcification due to fatty necrosis Fat density in CT Fat SI in MR T1 & T2: hyper intense appearing lipoma with both intra and extra cranial parts & defect in parietal bone

75. Discussion Considering such a wide range of differential diagnosis, firstly, it might be helpful to keep the mnemonic “HELP ME”. H= Hemangioma E = Epidermoid / dermoid L= Leptomeningeal cyst, Leukemia/Lymphoma P= Paget's disease, Postsurgical M= Metastases, Multiple Myeloma E= Eosinophilic granuloma , Encephalocele

76. Secondly, a careful evaluation of the margins of the lesion in conjunction with other imaging features, such as the number and the location, usually allows the Radiologist at least to state whether the lesion has benign or aggressive characteristics.

77. Benign lesions tend to have well-defined borders with sclerotic margins, a quite predictable location, mostly near the midline, and are usually solitary. On the other hand, those with a permeative appearance, multiple and randomly distributed, are probably aggressive.

78. After having ruled out typical normal variants, the benign versus aggressive imaging pattern should be consistent with the specific clinical indicators, the age of the patient being the first one to be taken into account. For instance, in adults and elderly patients, metastases are by far responsible for the majority of lytic skull lesions. children and young adults present more frequently one of the congenital, inflammatory, traumatic or benign neoplastic conditions mentioned above.

79. THANK YOU

80. QUESTIONS…. Approach to lytic lesions in skull Name few solitary & multiple lytic lesions Name few lytic lesions considering different age groups Imaging findings of dermoid cyst Imaging findings of fibrous dysplasia Imaging findings in calvarial osteomyelitis . Imaging findings in Multiple myeloma Suggestive features to differentiate multiple myeloma vs metastasis Importance of involvement of mastoid, mandible & sphenoid by LCH Common primaries of calvarial metastasis & importance of fat saturation in MR Meningioma vs hemangiopericytoma . Imaging findings in different phases of Pagets disease Normal variants of skull which present as lytic lesion Name bony defects that present as lytic lesion