PLAIN X-RAY SKULL – A SYSTEMATIC APPROACH

Presented By :

Dr Sameer Peer2ND Year PG Department of Radiodiagnosis

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.

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

Radiography

Skull SeriesBASIC:

• 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)

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

CollimationCollimate to outer margins of skull.

RespirationSuspend 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.)

TOWNE’S VIEW

Pathology DemonstratedSkull 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

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).

Lateral view

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).

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.

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.

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

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

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.

• Minimum SID is 40 inches (100 cm)

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.

Pathology DemonstratedOccipital bone, petrous pyramids, and foramen magnum, with dorsum sellae and posterior clinoids in its shadow

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.

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.

Facial bones and sinuses

There should be no rotation.

The petrous ridges must be below the floor of the maxilla.

Others…

Sella turcicaShuller’s view for TMJOptic ForaminaJugular foramen

…..and many more….

Approach to Skull X-rayThe various abnormalities that can be detected on plain skull X-ray can be categorized in the following groups :

1. Abnormal density2. Abnormal contour of the skull3. Abnormal intracranial volume4. Intracranial calcification5. Increased thickness of the skull6. Single lucent defect7. Multiple lucent defects8. Sclerotic areas

ABNORMAL DENSITYGeneralized 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

Osteogenesis Imperfecta Lacunar Skull

Osteopetrosis Fibrous dysplasia

ABNORMAL CONTOUR

NORMAL CONTOUR

SUTURES INTRACRANIAL CONTENTS

NEW BONE FORMATION

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.

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.

Sagittal synostosis Turricephaly(oxycephaly)

Plagiocephaly Harlequin eye – coronal synostosis

Cloverleaf skull

ACHONDROPLASIA

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

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

HAIR – ON END APPEARNCE

Single radiolucent Defect

Considerations while dealing with a single lucent lesion :

1. Location2. Associated soft tissue swelling3. Table of the bone involved 4. Margins – sharp, ill-defines, sclerotic

Causes of radiolucent defects :

5. Congenital – parietal foramina, anomalous apertures, meningoencephalocele, dermal sinus

6. Acquired – trauma, infections, tumors and histiocytosis.

Parietal Foramina

1. Rounded lytic defects2. Bilaterally symmetrical 3. Located in posterior parietal bone

Meningoencephalocele

4. Midline5. Frontal or occipital6. Sharp margins7. 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

• 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.

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

Paritel Foramina

DERMOID ENCEPHALOCELE

EPIDERMOID HEMANGIOMA

OSTEOMYELITIS

EOSINOPHILIC GRANULOMA

LINEAR SKULL FRACTURE GROWING FRACTURE

DEPRESSED FRACTURE

Multiple Radiolucent Defects

Children

• Craniolacunia• Wormian Bones• Increased Convolutional Markings• Histiocytosis• Metastasis – neuroblastoma, leukemia, Ewing’s Sarcoma

Adults

• Multiple Myeloma• Metastasis• Hyperparathyroidism

CRANIOLACUNIANEUROBLASTOMA – SUTURAL METASTASIS

NEUROBLASTOMA - METS

HAND-SCHULLER-CHRISTIAN METASTASIS

MULTIPLE MYELOMA HYPERPARATHYROIDISM

Wormian Bones Convolutional Markings – Copper Beaten Skull

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

OSTEOPETROSIS FIBROUS DYSPLASIA

OSTEOMA HYPEROSTOSIS

OSTEOPOROSIS CIRCUMSCRIPTA PAGET’S DISEASE

MENINGIOMA – HYPEROSTOSIS WITH PROMINENT VASCULAR MARKINGS

HYPEROSTOSIS FRONTALIS INTERNA

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

PINEAL CALCIFICATIONTUBEROUS SCLEROSIS

STURGE-WEBER SYNDROME Vein of Galen Aneurysm

SUPRA SELLAR CALCIFICATION - CRANIOPHARYNGIOMA

INTRACRANIAL CALCIFICATION - TORCHES

SUMMARY

1. Radiographic Positioning2. Age3. History/examination4. Biochemical/microbiological profile5. Detection of the abnormality6. Description of the abnormality –

Focal/generalized/abnormal shape/volume7. Lucent/sclerotic lesion – focal/generalized,

margins/soft tissue, physiological/pathological, associated findings

8. Formulate a differential diagnosis of 2-3 conditions

9. Further evaluation