Conventional X-ray Findings in various diseases

1. PLAIN X-RAY SKULL – A SYSTEMATIC
APPROACH
Presented By :
Dr Sameer Peer
2ND Year PG
Department of Radiodiagnosis

2. Introduction
• Skull radiographs were once considered an essential step in the evaluation of a
patient presenting with neurological signs and symptoms.
• The role of Plain X-ray skull has been redefined with the advent of CT and MRI.
• In patients presenting with stroke, epilepsy, dementia or in post-operative cases,
skull X-rays provide no useful information and MRI/CT is the investigation of
choice.

3. Major Indications of Skull radiographs
• Dysplasias
• Diagnostic survey in abuse
• Abnormal Head shapes
• Infections and tumors affecting the skull bones
• Metabolic bone disease
• Leukemia
• Multiple Myeloma
• Trauma – medico-legal case, may detect some linear fractures
• Detection of calcifications, hyperostosis , lytic/sclerotic metastasis

4. Radiography

5. Skull Series
BASIC:
• AP axial (Towne method)
• Lateral
• PA axial 15° (Caldwell method) or PA axial 25° to 30°
• PA 0°
SPECIAL :
• Submentovertex (SMV)
• PA axial (Haas method)

8. 1. Towne’s Method
Pathology Demonstrated
Skull fractures
Positioning
• IR size—24 × 30 cm (10 × 12 inches), lengthwise
• Moving or stationary grid
• 70 to 80 kV range
• Small focal spot
• Depress chin, bringing OML perpendicular to IR. For patients unable to flex
their neck to this extent, align the IOML perpendicular to the IR. Add
radiolucent support under the head if needed.
• Align midsagittal plane to CR and to midline of the grid or the table/Bucky
surface.
• Ensure that no head rotation and/or no tilt exists.
• Ensure that vertex of skull is in x-ray field

9. Collimation
Collimate to outer margins of skull.
Respiration
Suspend respiration.
If patient is unable to depress the chin sufficiently to bring the OML perpendicular to the IR
even with a small sponge under the head, the infraorbitomeatal line (IOML) can be placed
perpendicular instead and the CR angle increased to 37° caudad. This maintains the 30°
angle between the OML and the CR and demonstrates the same anatomic relationships. (A
7° difference exists between the OML and the IOML.)

10. TOWNE’S VIEW

11. Pathology Demonstrated
Skull fractures. A common general skull routine includes both right and left laterals.
Positioning
• Place the head in a true lateral position, with the side of interest closest to IR and
the patient's body in a semiprone position as needed for comfort.
• Align midsagittal plane parallel to IR, ensuring no rotation or tilt.
• Align interpupillary line perpendicular to IR, ensuring no tilt of head.
• Adjust neck flexion to align IOML perpendicular to front edge of IR

12. Central Ray
• Align CR perpendicular to IR.
• Center to a point 2 inches (5 cm) superior to EAM .
• Center IR to CR.
• Minimum SID is 40 inches (100 cm).

13. Lateral view

14. Pathology Demonstrated
Skull fractures (medial and lateral displacement)
Positioning
• Rest patient's nose and forehead against table/Bucky surface.
• Flex neck as needed to align OML perpendicular to IR.
• Align midsagittal plane perpendicular to midline of the grid or table/Bucky surface to
prevent head rotation and/or tilt.
• Center IR to CR.
Central Ray
• Angle CR 15° caudad and center to exit at nasion.
• Alternate with CR 25° to 30° caudad, and center to exit at nasion.
• Minimum SID is 40 inches (100 cm).

16. Alternate 25° to 30°: An alternate
projection is a 25° to 30° caudad tube
angle that allows better visualization of
the superior orbital fissures (black
arrows), the foramen rotundum (small
white arrows), and the inferior orbital rim
region. CR exits at level of nasion.
Structures Shown: • Greater and lesser
sphenoid wings, frontal bone, superior
orbital fissures, frontal and anterior
ethmoid sinuses, superior orbital
margins, and crista galli are shown.

17. Pathology Demonstrated
Skull fractures (medial and lateral displacement)
Positioning
• Rest patient's nose and forehead against
table/Bucky surface.
• Flex neck, aligning OML perpendicular to IR.
• Align midsagittal plane perpendicular to
midline of table/Bucky to prevent head
rotation and/or tilt (EAMs same distance from
table/Bucky surface).
• Center IR to CR.

18. Structures Shown: • Frontal bone,
crista galli, internal auditory canals,
frontal and anterior ethmoid sinuses,
petrous ridges, greater and lesser
wings of sphenoid

19. Warning: Rule out cervical spine fracture or subluxation on trauma patient before
attempting this projection

20. Positioning
• Raise patient's chin and
hyperextend the neck if possible until
IOML is parallel to IR.
• Rest patient's head on vertex.
• Align midsagittal plane
perpendicular to the midline of the
grid or table/Bucky surface, thus
avoiding tilt and/or rotation.
Central Ray
• CR is perpendicular to
infraorbitomeatal line.
• Center 1½ inch (4 cm) inferior to the
mandibular symphysis, or midway
between the gonions.
• Center image receptor to CR.
Structures Shown: • Foramen ovale and
spinosum, mandible, sphenoid and
posterior ethmoid sinuses, mastoid
processes, petrous ridges, hard palate,
foramen magnum, and occipital bone
are shown.

21. Pathology Demonstrated
Occipital bone, petrous pyramids, and foramen magnum, with dorsum sellae and
posterior clinoids in its shadow

22. Positioning
• Rest patient's nose and forehead against
the table/Bucky surface.
• Flex neck, bringing OML perpendicular to
IR.
• Align midsagittal plane to CR and to the
midline of the grid or table/Bucky surface.
• Ensure that no rotation or tilt exists
(midsagittal plane perpendicular to IR).
Central Ray
• Angle CR 25° cephalad to OML.
• Center CR to midsagittal plane to pass
through level of EAMs and exit 1½ inches
(4 cm) superior to the nasion.
• Center image receptor to projected CR.
• Minimum SID is 40 inches (100 cm).
Structures Shown: • Occipital bone, petrous
pyramids, and foramen magnum are
shown, with the dorsum sellae and
posterior clinoids visualized in the shadow
of the foramen magnum.

23. Water’s View
Positioning
Patient is seated facing the Bucky. Get the
chair as close to the Bucky as possible. May
also be taken standing.
Mentomeatal line should be perpendicular to
film with mouth closed.
The nose will be 1-2 cms from Bucky with
chin resting on Bucky.
The mouth may be opened to see the
sphenoid sinus. When this is done, the
canthomeatal line should be 35 to 40
degrees to the Bucky.

24. Facial bones and sinuses
There should be no rotation.
The petrous ridges must be below the floor of
the maxilla.

25. Others…
Sella turcica
Shuller’s view for TMJ
Optic Foramina
Jugular foramen
…..and many more….

26. Approach to Skull X-ray
The various abnormalities that can be detected on plain skull X-ray can be
categorized in the following groups :
1. Abnormal density
2. Abnormal contour of the skull
3. Abnormal intracranial volume
4. Intracranial calcification
5. Increased thickness of the skull
6. Single lucent defect
7. Multiple lucent defects
8. Sclerotic areas

27. ABNORMAL DENSITY
Generalized reduced density
• Osteogenesis Imperfecta
• Hypophosphatasia
• Achondrogenesis
Focal Reduced density
• Lacunar skull – focal areas of nonossified bone bound by normally
ossified bone
Generalized Increased density
• Osteopetrosis – basal bone initially, followed by calvaria
• Pyknodysostosis
Localized increased density
• Fibrous dysplasia
• Osteoma
• Craniometaphyseal dysplasia

28. Osteogenesis Imperfecta Lacunar Skull
Osteopetrosis Fibrous dysplasia

29. ABNORMAL CONTOUR
NORMAL CONTOUR
SUTURES
INTRACRANIAL
CONTENTS
NEW BONE
FORMATION

30. PREMATURE FUSION OF SUTURES
• Craniosynostosis
• Commonest cause of abnormal contour in children
• Calvarium expands to accommodate the growing brain in the axis of the
fused suture.
Scaphocephaly
• Sagittal synostosis
• Most common of the isolated synostosis
• M:F = 4:1
• Elongated narrow boat-shaped skull
Turricephaly
• Closure of both coronal sutures and lambdoid sutures
• Short, wide skull with towering head, bulging temporal areas and
shallow orbits
• The recessed supraorbital rims and hypoplasia of basal frontal
bones gives cloverleaf skull appearance.

31. Plagiocephaly
• Unilateral coronal or lambdoid synostosis
• Unicoronal synostosis is the second most common form of craniosynostosis
after sagittal synostosis.
• 2/3rd cases occur in females and 10% are familial
• There occurs elongation of the orbit, elevation of the lateral portion of the
ipsilateral orbital rim – the Harlequin eye appearance
• Tilting of the nasal septum and crista galli towards the ipsilateral side.
Expansion of bony calvarium due to presence of slow
growing intracerebral or sub arachnoid SOLs
• Arachnoid cysts
• Chronic SDH – calcifications may facilitated the diagnosis
Abnormal bone formation
• Achondroplasia – defective enchondral ossification
• Skull base is affected (develops from cartilage). Calvarium not affected (
membranous bones)
• Small foramen magnum, enlarged cranium, frontal bossing and large jaws.

32. Sagittal synostosis Turricephaly(oxycephaly)
Plagiocephaly Harlequin eye – coronal synostosis

33. Cloverleaf skull
ACHONDROPLASIA

34. ABNORMAL INTRACRANIAL VOLUME
• Abnormal cranial volume can be determined by measuring the skull directly and then
comparing the measurements to the standard for age and body size.
• Skull vault to face ratio. Volume of skull vault to face is 4:1 at birth, 3:1 by 2 years,
1.5:1 by adulthood.
Enalrged head size
• Hydrocephalus
• Macrocephaly
• Hydranencephaly
• Pitutary dwarfism
Small Skull
• Microcephaly – otherwise normal contour, associated with mental retardation.
• Sinuses are large and digital or convolutional markings are absent or decreased
• Sutures fuse early, but this is not the cause but a result of microcephaly
• D/D from premature fusion of sutures

35. Increased thickness of the skull
• Early cessation of brain growth
• Cerebral atrophy
• Hemolytic anemia – thalassemia, sickle cell, hereditary spherocytosis
• Progressive hydrocephalus
Hemolytic anemias – most striking in thalassemia. Diploic space is widened with striking
radial striations ( “hair – on –end”). PNS may be completely obliterated.
Progressive hydrocephalus
Without shunting – large bony calvarium decreased diploic space
With shunting – abnormal expansion ceases, arrested hydrocephalus, sutures close, inner
table thickens, diploic space widens

36. HAIR – ON END APPEARNCE

37. Single radiolucent Defect
Considerations while dealing with a single lucent lesion :
1. Location
2. Associated soft tissue swelling
3. Table of the bone involved
4. Margins – sharp, ill-defines, sclerotic
Causes of radiolucent defects :
1. Congenital – parietal foramina, anomalous apertures,
meningoencephalocele, dermal sinus
2. Acquired – trauma, infections, tumors and histiocytosis.

38. Parietal Foramina
1. Rounded lytic defects
2. Bilaterally symmetrical
3. Located in posterior parietal bone
Meningoencephalocele
1. Midline
2. Frontal or occipital
3. Sharp margins
4. Associated soft tissue swelling
Dermal Sinus
• Midline radiolucent defect
• Sharp, slightly sclerotic margin
• Associated lipoma or nevus of the overlying soft tissues
• Intracranial components – CT
Fractures
• At the site of injury associated with soft tissue swelling

39. • Linear nondepressed fractures – Radiolucent lines. Not to be confused with
vascular grooves ( ill-defined, undulant course) and sutures ( saw-toothed, expected
anatomical location)
• Depressed fractures – Area of increased radiodensity surrounded by a radiolucent
zone.
In children, arachnoid membrane may herniate through the torn dura and pulsations
lead to enlargement of the arachnoid collection resulting in Growing fracture.
Bulging membranes lead to the formation of a Leptomeningeal cyst.
Infections
• Rare
• Follow trauma or a spread from other sites
• Radiographically – mottled irregular lucencies which have well-defined borders and
associated swelling of the scalp.
Epidermoid tumors
• Congenital inclusion of epithelial cells within the calvarium
• Well-defined lytic lesions with sclerotic borders
• Not necessarily mid-line
• Intracranial epidermoids may produce a radiolucent shadow mimicking a lytic
lesion.

40. Malignant lesions
• Primary osteosarcoma – gross destruction of the bone with well defined margins
and soft-tissue component
• Metastasis
• Intacranial mass lesions may present as lytic skull lesion
Neurofibromatosis is a rare cause of lytic skull lesion – not due to neurofibroma,
but due to mesenchymal defect.
Histiocytosis X
( Eosinophilic granuloma, Letterer-Siwe disease, Hand-Schüller-Christian
disease)
• A single lytic lesion having sharp, non-sclerotic barder and bevelled edges is
characteristic of eosinophilic granuloma.
• A small bone in the center – Button sequestrum.
• Other two variants have larger, multiple and punched out lesions

41. Paritel Foramina
DERMOID ENCEPHALOCELE

42. EPIDERMOID HEMANGIOMA
OSTEOMYELITIS

43. EOSINOPHILIC
GRANULOMA

44. LINEAR SKULL FRACTURE GROWING FRACTURE
DEPRESSED FRACTURE

45. Multiple Radiolucent Defects
Children
• Craniolacunia
• Wormian Bones
• Increased Convolutional Markings
• Histiocytosis
• Metastasis – neuroblastoma, leukemia, Ewing’s Sarcoma
Adults
• Multiple Myeloma
• Metastasis
• Hyperparathyroidism

46. CRANIOLACUNIA
NEUROBLASTOMA – SUTURAL METASTASIS
NEUROBLASTOMA - METS

47. HAND-SCHULLER-CHRISTIAN METASTASIS
MULTIPLE MYELOMA HYPERPARATHYROIDISM

48. Wormian Bones Convolutional Markings – Copper Beaten Skull

49. Sclerotic Areas of Skull
• Osteopetrosis
• Fibrous Dysplasia – Sclerotic lesion with loss of trabecular pattern/ mixed lesions
• Paget’s Disease – “Cotton wool” skull, thickening of diploic space, enlargement,
osteoporosis circumscripta
• Osteoma
• Proteus Syndrome – hyperostosis
• Meningioma – hyperostosis
• Hyperostosis frontalis interna – elderly, inner table, does not cross midline, spares
diploic space

50. OSTEOPETROSIS FIBROUS DYSPLASIA
OSTEOMA HYPEROSTOSIS

51. OSTEOPOROSIS CIRCUMSCRIPTA PAGET’S DISEASE

52. MENINGIOMA – HYPEROSTOSIS WITH PROMINENT VASCULAR MARKINGS
HYPEROSTOSIS FRONTALIS INTERNA

53. INTRACRANIAL CALCIFICATION
Physiological – Pineal, Choroid plexus, Habenular, basal ganglia, falcine, anterior
petroclinoid ligaments, pitutary (rare), ICA.
Abnormal –
• Familial – Tuberous Sclerosis, Sturge-Weber Syndrome, Idiopathic familical
cerebrovascular calcinosis (Fahr’s)
• Metabolic – Hypoparathyroidism, Pseudohypoparathyroidism,
Hyperparathyroidism
• Inflammatory – CMV, Toxoplasmosis, Rubella, Abscess
• Vascular – AVM, Aneurysm, Hematoma
• Neoplasm – Craniopharyngioma, Astrocytoma, oligodendroglioma, pinealoma

54. PINEAL CALCIFICATION
TUBEROUS SCLEROSIS
STURGE-WEBER SYNDROME Vein of Galen Aneurysm

55. SUPRA SELLAR CALCIFICATION -
CRANIOPHARYNGIOMA
INTRACRANIAL CALCIFICATION - TORCHES

56. SUMMARY
1. Radiographic Positioning
2. Age
3. History/examination
4. Biochemical/microbiological profile
5. Detection of the abnormality
6. Description of the abnormality –
Focal/generalized/abnormal shape/volume
7. Lucent/sclerotic lesion – focal/generalized,
margins/soft tissue, physiological/pathological,
associated findings
8. Formulate a differential diagnosis of 2-3
conditions
9. Further evaluation