Thick Skull, Generalized
Miral D. Jhaveri, MD
DIFFERENTIAL DIAGNOSIS
Common
Skull Normal Variants
Diffusely Thick Skull, Normal
Hyperostosis Frontalis Interna
Phenytoin (Dilantin) Use, Chronic
Shunted Hydrocephalus
Metastases (Diffuse Sclerotic)
Paget Disease
Less Common
Microcephaly
Fibrous Dysplasia
Hyperparathyroidism
Acromegaly
Subdural Hematoma, Chronic (Calcified)
Anemias
Iron Deficiency Anemia
Sickle Cell Disease
Thalassemia
Extramedullary Hematopoiesis
Rare but Important
Sclerosing Bone Dysplasias
Osteopetrosis
Pycnodysostosis
Melorheostosis
Fluorosis
ESSENTIAL INFORMATION
Key Differential Diagnosis Issues
Diffuse diploic space expansion with/without adjacent cortical thickening
Most common cause by far of “thick skull” = normal variant!
Helpful Clues for Common Diagnoses
Skull Normal Variants
Most common cause
Females normally have significantly thicker parietal/occipital bones than males
Hyperostosis frontalis interna
Usually bilateral, symmetrical
Spares areas occupied by superior sagittal sinus, cortical venous channels
Often ends at coronal sutures
May extend to parietal bones, orbital roofs
Females > 35 years old
No clinical significance
Etiology unknown
Phenytoin (Dilantin) Use, Chronic
Look for combination of thick skull + cerebellar atrophy = probable chronic Dilantin therapy
Up to 34% among patients with seizure disorder + anticonvulsant therapy
Shunted Hydrocephalus
Chronic shunted hydrocephalus often associated with diffuse calvarial thickening
Look for thick skull + shunt + chronic collapsed ventricles
Metastases (Diffuse Sclerotic)
Fat-suppressed T1 C+ scans helpful in detecting calvarial, subtle dural metastases
Common with prostate & breast metastasis
Look for associated focal/diffuse dura-arachnoid involvement
Paget Disease
Initial osteolytic change of skull in osteoporosis circumscripta
Late osteosclerotic phase
Osteoblastic areas crossing sutures
Marked thickening of the diploic space
“Tam-o’-shanter” skull
Focal areas of sclerosis in expanded diploic space: “Cotton wool” appearance (of skull)
Platybasia with basilar invagination
Helpful Clues for Less Common Diagnoses
Microcephaly
Skull overgrowth occurs secondary to small brain
Small brain causes = developmental anomalies or a result of very early insult
Fibrous Dysplasia
Can involve any aspect of skull
Can be focal or extensive
Medullary expansion with ground-glass appearance is classic
Four disease patterns
Monostotic (70-80%)
Polyostotic (20-30%)
Craniofacial (can be isolated; up to 50% of polyostotic)
Cherubism (mandible, maxilla)
Hyperparathyroidism
Granular appearance of skull with multiple areas of normal bone interspaced between
“Salt & pepper” or “pepper pot skull” appearance
Loss of distinction of inner & outer table
Loss of lamina dura
Brown tumors
Chronic renal disease: Secondary hyperparathyroidism
↑ Serum calcium, ↑ parathyroid hormone, ↓ serum phosphorus
Acromegaly
Calvarial hyperostosis (esp. inner table)
Prognathism (elongation of mandible)
Sellar enlargement, erosion
Enlarged paranasal sinuses (mainly frontal): 75%
↑ Growth hormone & IGF-1
Subdural Hematoma, Chronic (Calcified)
Chronic calcified subdural hematoma along inner table simulates thick skull
Look for subtle cleavage between calcified membranes and the inner tableStay updated, free articles. Join our Telegram channel
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