skull pathologies

1. SKULL PATHOLOGIES ON
PLAIN RADIOGRAPHS
Dr.Sachin Babanagar
Assistant Professor , Dept of Radio-diagnosis,
DY Patil Hospital , Kolhapur

2. 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

3. 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

4. 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

5. Osteogenesis Imperfecta Lacunar Skull
Osteopetrosis Fibrous dysplasia

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

7. 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.

8. 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.

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

10. Cloverleaf skull
ACHONDROPLASIA

11. 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

12. 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

13. HAIR – ON END APPEARNCE

14. 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.

15. 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

16. • 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.

17. 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 edgesis
characteristic of eosinophilic granuloma.
• A small bone in the center – Button sequestrum.
• Other two variants have larger, multiple and punched out lesions

18. Paritel Foramina
DERMOID ENCEPHALOCELE

19. EPIDERMOID HEMANGIOMA
OSTEOMYELITIS

20. EOSINOPHILIC
GRANULOMA

21. LINEAR SKULL FRACTURE GROWING FRACTURE
DEPRESSED FRACTURE

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

23. CRANIOLACUNIA
NEUROBLASTOMA – SUTURAL METASTASIS
NEUROBLASTOMA - METS

24. HAND-SCHULLER-CHRISTIAN METASTASIS
MULTIPLE MYELOMA HYPERPARATHYROIDISM

25. Wormian Bones Convolutional Markings – Copper Beaten Skull

26. 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

27. OSTEOPETROSIS FIBROUS DYSPLASIA
OSTEOMA HYPEROSTOSIS

28. OSTEOPOROSIS CIRCUMSCRIPTA PAGET’S DISEASE

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

30. 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

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

32. SUPRA SELLAR CALCIFICATION -
CRANIOPHARYNGIOMA
INTRACRANIAL CALCIFICATION - TORCHES

33. THANK YOU