Physiologic and Age-Related
•Pineal gland
–Occurs in 2/3 of adult population
–Amorphous or ring-like calcifications,
under 3mm from midline,
usually under 10mm in diameter Fig. 1
–Caveat: pineal calcification over 14 mm is concerning for pineal neoplasm
•Habenula
–Occurs in 1/3 population
–Posteriorly open C-shaped calcification 4-6mm anterior to pineal gland Fig. 1
•Choroid plexus
–May calcify in all ventricles – most commonly in the lateral ventricle atria,
near the foramen of Monro and roof of the 4th ventricle Fig. 1
•Basal ganglia
–Incidental calcification may be faint and punctate,
or coarse and trabeculated
–Calcification may have a pathological cause,
possibly metabolic or endocrine in origin- to be considered in patients under the age of 40
•Falx cerebri/Tentorium cerebelli/Dura mater Fig. 1 Fig. 2
–Occurs in 10% of population
–May be incidental or can occur with a range of pathological conditions including basal cell naevus syndrome and pseudoxanthoma elasticum
–The petroclinoid ligament can calcify in the same way as other dural reflections Fig. 2
Vascular
•Arteriosclerosis Fig. 3
–Commonly seen in conjunction with atherosclerosis elsewhere in patients with vascular risk factors
–Usually linear or punctate calcification associated with the larger intracranial arteries- especially the basilar and vertebral arteries and the intra-cavernous internal carotid arteries
•Intracranial aneurysm Fig. 4
–Saccular dilatations of intracranial arteries,
commonly located at bifurcations
–Unenhanced CT usually shows hyperdense rounded abnormality adjacent to the parent vessel.
The most common pattern of calcification exhibited is curvilinear calcification at the periphery
–Increased incidence of calcification as the aneurysm size increases
–Thrombosed aneurysms may be entirely calcified
•Classical arteriovenous malformation Fig. 5 Fig. 6 Fig. 7
–Classical parenchymal or pial arteriovenous malformation consist of a nidus which forms a transition between a feeding artery and draining vein,
without an intervening capillary bed
–Unenhanced CT may show only slightly hyperdense nidus of serpentine vessels.
There may be curvilinear or punctate vascular calcification as in normal arteriosclerosis
–Pial AV malformations may also be associated with dystrophic calcifications in the adjacent cortex which is postulated to be due to ischaemia secondary to a “steal” phenomenon
•Cavernoma Fig. 8 Fig. 9 Fig. 10 Fig. 11 Fig. 12 Fig. 13 Fig. 14
–Also known as cavernous venous malformation or cavernous haemangioma
–Pathologically these lesions are a non-neoplastic clusters of dilated,
thin-walled capillaries with surrounding haemosiderin
–Usually solitary and supratentorial (80%)
–May not be visible on unenhanced CT.
Alternatively a round hyperdense intraparenchymal lesion may be seen,
which can show a central,
coarse popcorn-like pattern of calcification
–Rarely these lesions are familial and multiple,
and can be associated with haemorrhage Fig. 15
•Subdural Haematoma Fig. 16 Fig. 17 Fig. 18
–Chronic subdural haematomas are commonly seen and unenhanced CT shows a crescenteric extra-axial collection,
which is of varying density depending on the age of the haematoma.
Most commonly they are almost isodense to CSF
–Upto 10% of chronic subdural haematomas develop calcification,
most commonly linear calcification over the cerebral convexity surface
•Calcified Cerebral Embolus Fig. 19
–A rare cause of ischaemic stroke
–Sources of calcified emboli include calcified aortic stenosis,
atherosclerotic plaques in the carotid,
brachiocephalic or vertebral arteries and calcified mitral annulus
–Demonstrated as round or ovoid calcifications,
(density around 160HU),
in comparison to typical thrombi which have a tubular shape and are less dense (50-70HU)
–Most commonly seen in the middle cerebral artery
–Important to recognise,
as these patients are thought to have a higher rate of recurrent stroke; patients therefore require thorough investigation for the cause
•Ischaemic Stroke Fig. 20
–Calcification after ischaemic stroke is rare and tends to be discovered years after the acute event; this process may be accelerated in patients who have chronic renal failure or hyperparathyroidism
–CT shows gyriform cortical calcification in the arterial territory affected at the time of the infarct
Tumours
•Meningioma Fig. 21 Fig. 22 Fig. 23 Fig. 24
–Most common non-glial tumour of CNS and most common extra-axial neoplasm
–Accounts for ~15% of all intracranial tumours
–Typical CT features are of a well-defined,
hyperdense unilobular mass with a broad-based dural attachment.
Following contrast there is homogenous enhancement
–Usually occur over the cerebral convexities or in the parasagittal or sphenoid wing regions
–20-30% of meningiomas exhibit calcifications
–Calcification patterns may be sand-like/psammomatous,
focal/punctate,
diffuse and dense or rim-like
•Oliodendroglioma Fig. 25 Fig. 26 Fig. 27
–Typically manifest as sharply marginated round or oval mass that involves the cortex or subcortical white matter
–Usually hypodense (60%)
–Calcification is exhibited in up to 91% of cases,
this is usually coarse in morphology
•Craniopharyngioma Fig. 28 Fig. 29
–Relatively benign neoplasm that typically arises in the suprasellar region but can occur anywhere along the infundibulum
–Two distinct pathological types: adamantinomatous which tends to occur in the paediatric population and papillary which occurs in adults.
–Adamantinomatous craniopharyngiomas are more heterogenous in their CT appearances: they exhibit single or multiple cysts,
but can have enhancing soft tissue components.
90% of these tumours show calcification which is typically stippled and peripheral in location
–Papillary craniopharyngiomas are more spherical and usually lack a prominent cystic component.
Calcification is rare in the papillary subtype
•Pilocytic astrocytoma Fig. 30 Fig. 31
–Low-grade astrocytoma that tends to occur in young patients
–CT commonly shows a well demarcated large cystic component with a brightly enhancing mural nodule
–Tumour calcification is atypical,
and tends to be fleck-like.
It occurs most commonly in pilocytic astrocytomas of the hypothalamic region or the optic nerve
•Brain metastases Fig. 32
–Brain metastases rarely contain any calcification; one series reported occurrence in under 6% of cases
–Calcification can be punctate,
dense,
diffuse or curvilinear
–Can occur in metastases from a range of primary tumours,
including breast carcinoma,
adenocarcinoma of the lung,
mucinous GI adenocarcinoma,
sarcomas e.g.
osteosarcomas and ovarian tumours
–It can also occur in previously non-calcified metastases as a result of treatment e.g.
lymphoma and breast cancer
•Choroid plexus papilloma Fig. 33
–Benign intraventricular tumour which is more common in the paediatric population
–In children choroid plexus papillomas more commonly occur in the lateral ventricles,
with a predilection for the trigone,
whereas in adults it tends to be found in the 4th ventricle
–CT shows a well-defined,
lobulated mass which is usually isodense or slightly hyperdense
–Fine,
speckled calcification is seen in approximately 25% of cases
•Pineal region tumours Fig. 34 Fig. 35
–Normal prevalence of pineal calcification is 40% at CT,
this is almost always homogenous and dense.
This needs to differentiated from calcification associated with pineal neoplasms
–Pineal parenchymal tumours (e.g.
pineocytoma and pineoblastoma) tend to peripherally disperse normal calcifications,
while pineal germ cell tumours tend to engulf them
–Pineal germinomas are the most common pineal germ cell tumour; these tend to be homogenous masses which are slightly hyperdense and engulf the pineal gland,
which is calcified in almost 100% of cases Fig. 36 Fig. 37
–CT features of pineocytomas and pineoblastomas show considerable cross-over and it is difficult to differentiate them on imaging alone
•Ependymoma Fig. 38 Fig. 39
–More common in the paediatric population
–Posterior fossa (4th ventricle) is the most typical location
–Unenhanced CT shows well-defined,
lobulated mass,
which is slightly hyperdense or isodense
–Calcification,
ranging from small and punctate to large masses,
is common (upto 80% of cases)
•Intracranial Teratoma Fig. 40 Fig. 41
–Extragondal teratomas are thought to arise from misplaced,
pluripotential,
primordial germ cells
–The most common locations are the cerebral hemispheres and pineal/suprasellar region
–Hemispheric teratomas tend to present in the newborn and are larger; they are multi-loculated lesions which typically show intralesional fat and solid calcification
–Pineal/suprasellar region teratomas tend to occur in older children or young adults and also show regions of fat and clump-like calcification
•Dermoid of CNS Fig. 42 Fig. 43
–Strictly not a tumour,
but a congenital ectodermal inclusion cyst
–Most common intracranial locations are the posterior fossa and posterior to the superior orbital fissure
–CT shows a thick-walled,
inhomogenous mass with focal areas of fat,
often containing plaques of calcification
•Epidermoid Cyst
–As with dermoid cyst,
not actually a tumour but a congenital ectodermal inclusion cyst
–Commonest location is at the cerebellopontine angle
–CT shows a CSF-like mass that insinuates itself within cisterns,
encasing adjacent nerves and vessels
–Peripheral calcification is present in 10-25% cases
•Chordoma Fig. 44 Fig. 45
–Arises from embryonic remnants of the notochord
–Most commonly found at the sacrum,
but 35% occur in the clivus
–CT shows a low attenuation soft tissue mass with a high density fibrous pseudocapsule
–Calcification is common,
occurring in 50-75% of cases and is amorphous in appearance; these may represent sequestra of normal bone rather than dystrophic calcifications
•Chondrosarcoma
–Rare when compared with other skull base tumours
–Commonest locations include petro-occipital synchondrosis,
spheno-ethomoidal junction and sella turcica
–CT shows a soft tissue mass with disruption of the cortex,
a high proportion (~90%) show punctate areas of chondroid calcification
Infection
•TORCH Fig. 46 Fig. 47 Fig. 48
–Group of congenital infections consisting of Toxoplasmosis,
Other (syphilis,
varicella-zoster,
parvovirus B19),
Rubella,
Cytomegalovirus and Herpes
–Variety of effects on the foetal brain; CMV and Toxoplasmosis are most commonly associated with cerebral calcifications
–CMV tends to produce periventricular calcifications which are thick and chunky.
Elsewhere,
as in the basal ganglia,
the calcification is fine and punctate
–CMV may also cause migrational abnormalities,
white matter disease,
periventricular cysts,
cerebral atrophy,
ventriculomegaly and lenticulostriate vasculopathy
–Congenital Toxoplasmosis tends to produce calcifications predominantly in the basal ganglia and at the corticomedullary junction
•Neurocysticercosis Fig. 49 Fig. 50
–Common disorder worldwide due to encysted larvae of the tapeworm Taenia solium,
which develops after ingestion of ova from the faeces of a tapeworm carrier
–Larval cysts may be found in the subarachnoid space,
in the brain parenchyma (at the grey-white matter junction or in the basal ganglia) or within the ventricular system
–Earlier stages in the disease process (noncystic,
vesicular,
colloidal vesicular and granular nodular stages) show a variety of imaging features but no calcification
–Calcified nodular stage occurs when the parasite has died and there is a inflammatory response with subsequent calcification
–Imaging shows numerous completely calcified nodules in the parenchymal form of the disease
•Tuberculosis
–CNS TB infection may affect any intracranial compartment and manifestations include meningitis (lepto- and pachy-),
tuberculous granuloma,
abscess,
rhombencephalitis and encephalopathy
–Tuberculous leptomeningitis is the most common CNS manifestation overall
–Tuberculous granuloma (tuberculoma) is the most common parenchymal lesion of TB
–Tuberculomas may be solitary,
multiple or miliary and may be found anywhere in the brain parenchyma
–Tuberculomas may be isodense,
hyperdense of mixed density and can show peripheral enhancement
–Calcification may occur as a central nidus within the tuberculoma with a low density rim (+/- rim enhancement – “the target sign”),
or later in the disease course when the tuberculoma is entirely calcified
Neurocutaneous Syndromes
•Tuberous sclerosis Fig. 51 Fig. 52
–Autosomal dominant inherited syndrome characterised by hamartomatous lesions in a variety of organs
–Intracranial manifestions include cortical tubers,
subependymal hamartomas,
subependymal giant cell astrocytomas (SGCA) and white matter abnormalities
–Intracranial calcification may be seen with cortical tubers (mass-like or curvilinear,
in 50% by 10 years),
SGCA or subependymal hamartomas (dense calcification)
•Sturge-Weber Syndrome Fig. 53 Fig. 54
–Rare,
sporadic neurocutaneous syndrome
–Almost always associated with congenital facial cutaneous haemangioma in a territory supplied by a trigeminal nerve branch (most commonly V1- opthalmic division)
–Associated leptomeningeal angioma causes vascular steal from the subjacent cortex and white matter with resultant local ischaemia
–CT shows atrophy of the affected area of brain with “tram-track” gyriform calcifications; there may also be associated enlargement of the regional venous sinus and ipsilateral choroid plexus
•Neurofibromatosis type 1
–Most common neurocutaneous syndrome.
May be inherited in an autosomal dominant manner or develop as a sporadic mutation
–Intracranial manifestations include a range of neoplasms,
sphenoid wing dysplasia,
lambdoid suture defects,
dural calcification at the vertex and rarely moya-moya phenomenon
–Calcifications tends to occur in association with neoplasms e.g.
ganglioglioma or pilocytic astrocytoma
•Neurofibromatosis type 2
–Rare neurocutaneous syndrome
–Intracranial calcification most commonly associated with multiple meningiomas,
ependymomas or schwannomas
•Gorlin-Goltz Syndrome Fig. 55
–Also known as basal cell naevus syndrome
–Rare phakomatosis
–Characterised by basal cell carcinomas,
odontogenic keratocytes,
palmar+/- plantar pits,
skeletal abnormalities,
prognathism and calcification of the falx cerebri and tentorial leaflets.
–Patients are also predisposed to a range of malignancies,
including medulloblastoma,
meningioma,
fibrosarcoma and cardiac fibroma.
Metabolic and Endocrine
•Fahr Disease Fig. 56
–Also known as bilateral striatopallidodentate calcinosis
–Rare neurodegenerative disease
–Characterised by bilateral,
symmetric deposition of calcium and other minerals in the basal ganglia,
thalami,
dentate nuclei and centrum semiovale
–CT shows bilaterally symmetric dense calcifications in the basal ganglia,
dentate nuclei,
thalamus and subcortical white matter
–Radiological differential diagnosis included hypoparathyroidism,
pseudo- and pseudopseudohypoparathyroidism Fig. 57
Radiation Induced
•Mineralising microangiopathy Fig. 57 Fig. 58 Fig. 59
–Usually follows combined radiation and chemotherapy for treatment of CNS neoplasms in childhood
–Occurs after a latent period
–CT generally shows punctate calcification in the basal ganglia
–Calcification may also occur in the subcortical white matter and dentate nuclei