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Intracranial calcificitation on CTDr K KABULO

Introduction Knowledge of physiologic calcifications in the brain parenchyma is essential to avoid misinterpretations. Several pathologic conditions involving the brain are associated with calcifications and the recognition of their appearance and distribution helps to narrow the differential diagnosis.

Noncontrast-enhanced CT of the head is the preferred imaging modality over MRI.MRI is quite risky may miss faint calcification.

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intracranial calcifications can be classified mainly into 6 groups based on their etiopathogenesis: age-related and physiologic, congenital, infectious, endocrine and metabolic, vascular, and neoplastic

The pathogenesis of intracranialcalcification remains unknown. Possible determinants ofextra-osseous calcification include the calcium phos-phate product, metabolic acidosis, local pH change,expression of osteopontin and matrix Gla protein, andinflammation or tissue injury.

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Age-related physiologic and neurodegenerative calcifications

Intracranial physiologic calcifications are unaccompanied by any evidence of disease and have no demonstrable pathological cause

Normal intracranial calcificationscan be defined as all age-related physiologic and neurodegenerative calcifications that are unaccompanied by any evidence of disease and have no demonstrable pathological cause.physiologic calcification are extremely common incidental discovered, with almost no clinically significance5

Physiologic calcifications may appear as: hyperdense flat plaques (falx cerebri), laminar (dural, tentorial, petroclinoid ligament, superior sagittal sinus), curvilinear (habenula, epiphysis), faint punctate or have coarse conglomerated pattern (basal ganglia)

The typical location are:the epiphysis Pineal glandhabenulachoroid plexus,tentoriumpetroclinoid ligamentsfalx cerebribasal gangliasagittal sinus.

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Calcification of the pineal gland55% of patients> 20 yrs age have a calcified pineal gland visible on plain skull x-rayseen in two-thirds of the adult population and increases with age. Pineal calcification over 1 cm in diameter or under 9 years of age may be suggestive of a neoplasm

Causes of Pineal Gland CalcificationAs noted above, calcification tends to become more severe with age, with many people experiencing symptoms of heavy calcification of the pineal gland by the time they are 17. This means that an MRI or other scan would show a large lump of calcium phosphate on the gland as well as other parts of the body.This calcification process is caused by constant exposure to substances like fluoride which build up in the body over time. Toothpaste, public water systems, hormones, food additives, excess sugar and sweeteners in your diet or even regular exposure to cell phones has been linked to the phenomenon of calcifying the pineal gland.

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Causes of Pineal Gland CalcificationAs noted above, calcification tends to become more severe with age, with many people experiencing symptoms of heavy calcification of the pineal gland by the time they are 17. This means that an MRI or other scan would show a large lump of calcium phosphate on the gland as well as other parts of the body.This calcification process is caused by constant exposure to substances like fluoride which build up in the body over time. Toothpaste, public water systems, hormones, food additives, excess sugar and sweeteners in your diet or even regular exposure to cell phones has been linked to the phenomenon of calcifying the pineal gland.

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Habenula calcification

it has a central role in the regulation of the limbic system and is often calcified with a curvilinear pattern a few millimeters anterior to the pineal body in 15% of the adult population

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Note pineal gland and habenular calcification in this patient with chronic bifrontal hygromas.11

Choroid plexus calcification

Very common finding, usually in the atrial portions of the lateral ventriclesit is visualized nine to 15 times more frequently with computed tomography (CT) than with plain skull radiography. Calcification involving the temporal horns is associated with neurofibromatosis

choroid plexus: the most common site for physiologic calcification (in lateralventricles where it is usually bilateral and symmetric; rare in 3rd & 4thventricles). Increases in frequency and extent with age (prevalence: 75% by5th decade). Rare under age 3. Under age 10, consider possible choroid plexuspapilloma. Involvement in the temporal horns is often associated withneurofibromatosis12

Calcification in the third or fourth ventricle

Calcification in the third or fourth ventricle or in patients less than 9 years of age is uncommon.

Basal ganglia calcificationsUsually idiopathic incidental findings that have a 0.31.5% incidence and increases with age. They usually demonstrate a faint punctuate or a coarse conglomerated symmetrical calcification pattern

basal ganglia (BG): slight bilateral BG calcifications on CT are common, especiallyin the elderly. Considered a normal radiographic variant by some.They may be idiopathic, secondary to conditions such as hypoparathyroidismor long-term anticonvulsant use, or part of rare conditions such asFahr's disease(The disease was first noted by German neurologist Karl Theodor Fahr in 1930: progressive idiopathic calcification of medial portions of basalganglia, sulcal depths of cerebral cortex, and dentate nuclei). BG calcifications> 0.5 em dia are possibly associationwith cognitive impairment and a high prevalence of psychiatricsymptoms116

basal ganglia (BG): slight bilateral BG calcifications on CT are common, especiallyin the elderly. Considered a normal radiographic variant by some.They may be idiopathic, secondary to conditions such as hypoparathyroidismor long-term anticonvulsant use, or part of rare conditions such asFahr's disease(The disease was first noted by German neurologist Karl Theodor Fahr in 1930: progressive idiopathic calcification of medial portions of basalganglia, sulcal depths of cerebral cortex, and dentate nuclei). BG calcifications> 0.5 em dia are possibly associationwith cognitive impairment and a high prevalence of psychiatricsymptoms117

Calcifications of the falx, dura mater or tentorium cerebelli

occur in about 10% of elderly population.Falcian calcifications usually have a characteristic appearance pattern as dense and flat plaques and are usually seen in the midline of the cerebrumDural and tentorial calcifications are usually seen in a laminar pattern and can occur anywhere within the cranium

Dural calcifications: Very common in older age groups and are usually located in the falx or the tentorium, usually few. Presence ofmultipleand extensive dural calcifications or duralcalcificationin children should raise the suspicion of underlying pathology.19

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Petroclinoid ligament and sagittal sinus calcifications are common age-related degeneration sites and usually have laminar or mildly nodular patterns

The petroclinoid ligaments are a fold of the dura mater that extends between the anterior and posterior clinoid processes and the petrosal part of the temporal bone.Thus there are two separate bands, which are termed the anterior and posterior petroclinoid ligaments respectively. The anterior petroclinoid ligament is considered to be an extension of the tentorium cerebelli, while the posterior petroclinoid ligament arises from posteromedial extensions of the tentorial notch.The petroclinoid ligament may calcify as other structures that you can see in normal intracranial calcifications.

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Congenital calcificationsThis condition is frequently seen :

in Sturge-Weber syndrome (SWS), tuberous sclerosis (TS) and intracranial lipoma, but rarely in neurofibromatosis(NF), Cockayne (CS) and Gorlins syndromes (GS).

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Tuberous sclerosiscortical/subcortical hamartomas.The subcortical tubers are usually supratentorial, and they calcify mostly in elderly patients.subependymal nodules.Calcified subependymal hamartomas are found mostly along the lateral ventricles and may appear as localized projections into the ventricular cavity.

TS is an autosomal dominant disorder characterized by mental retardation, epilepsy and adenomasebaceum. Intracranial lesions in TS consist of subependymal hamartomas, subcortical tubers, giant cell tumors,and white matter lesions.

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Sturge-Weber syndrom

dense gyriform cerebral calcifications often affect the parietal-occipital cortical areas or choroid plexus;

diffuse high attenuation of the superficial and deep white matter, presumably due to microcalcifications;

SWS is a rare disorderconsisting of a port-wine nevus in the distribution of the ophthalmicbranch of the trigeminal nerve and nervous system malformations. Thesyndrome results from malformation of the cerebral vasculature locatedwithin the pia mater. This malformation leads to venous hypertensionand subsequent hypoperfusion of the underlying cortex, causing chroniccerebral ischemia, parenchymal atrophy, enlargement of the ipsilateralchoroid plexus and calcification. Calcification in SWS demonstrates acharacteristic linear cortical pattern (3) (Fig. 6).

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brain atrophy; thickening of the calvaria--as an indirect feature of loss of the brain substance;gyriform enhancement--reflecting pial angiomatosis.

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Neurofibromatosis type I.enlarged optic nerve foramina and fissure and dural calcification, explained by the association of different intracranial tumors, such as optic nerve glioma and plexiform neurofibroma.

Neurofibromatosis type IIIntracranial calcifications are:non tumoral--mainly nodular calcifications of the cerebellum, symmetric or often asymmetric calcifications of the choroid plexus and seldom cortical calcifications or associated with disease-related tumors, such as meningiomas or ependymomas.

Vascular disorders

Intracranial atherosclerosis is emphasized by the presence of linear or punctate arterial wall calcifications of large intracranial vessels, affecting mainly the carotid and middle cerebral arteries and the vertebro-basilar system.

Other causes of vascular intracranial calcifications are:Aneurysm: thrombosed aneurysm commonly presents calcifications with rim-like and granular pattern

Arteriovenous malformation

iso/hyperdense serpentine vessels; multiple curved or punctate vascular calcifications; and vascular tracks with prevalence peripheral location and strong enhancement.

Arterio-venous malformation. Right frontal lobe heterogeneous lesion: (a) withsmall hypodense central area, multiple serpentines vascular calcification (white arrows),(b) intense enhanced vascular tracks located peripheral (red arrows).36

Developmental venous anomalyrepresented by dilated medullary white matter veinswith "medusa head" aspect. CT features:occasional small punctate calcification;enhancing stellate tubular vessels converging in collector vein.

Developmental venous anomaly. Right cerebellar hemisphere heterogeneouslesion with small hypodense central area, multiple serpentines vascular calcification(red arrows), vascular tracks with "medusa head" sketch located peripheral with intenseenhancement (white arrows).38

Cavernous malformation are usually smaller than 3 cm, well defined hyperdense masses, without causing mass effect, sometimes partially calcified. After intravenous contrast administration there is little or no enhancement.Vein of Galen aneurysms may appear on non-enhanced CT as mildly hyperdense venous pouch with wall calcifications, hydrocephalus and parenchymal calcification.

Cavernous malformation. (a) NECT Small hyperintens lesion, with punctatecalcification in left periventricular white matter, near occipital lateral ventricle horn.(b )MRI. "Pop-corne" appearance with hipointense hemosiderin rim on T2-wi (greenarrow); T1-wi with Gd - shows small venous malformation associated (white arrow).40

Infection cysticercosisencephalitis, meningitis, cerebral abscess (acute and healed)granuloma (torulosis and other fungi)hydatid cysttuberculomaparagonimiasisrubellasyphilitic gumma

Paragonimus is a lung fluke (flatworm) that infects the lungs of humans after eating an infected raw or undercooked crab or crayfish. Less frequent, but more serious cases of paragonimiasis occur when the parasite travels to the central nervous system.41

InfectionsCongenitalCytomegalovirus and toxoplasmosis infections are commonly associated with hydrocephalus and randomly periventricular, subependymal, basal ganglia and cerebral cortical nodular calcifications.Infection with immunodeficiency virus results in periventricular, frontal white-matter and cerebellar calcifications.

Congenital herpes (HSV-2) infections present punctate or extensive gyral calcification, thalamic and periventricular calcification, also extensive cerebral destruction and multicystic encephalomalacia

Acquired Cysticercosis.Typical appearance is that of a small calcified cyst with eccentric calcified nodule, representing the dead scolex. The most frequent calcifications locations are in the brain parenchyma, especially the gray-white matter junction and subarachnoid spaces in the convexities, ventricles, and basal cisterns

Cryptococcosis affects immunocompromised patients. Calcifications can be present in both the brain parenchyma and the leptomeninges. HIV.Calcifications may be seen in basal ganglia in patients with HIV encephalitis

Tuberculosis. Calcified parenchymal tuberculoma can occur in intracranial tuberculosis. The "target sign" formed by the calcified central nidus with peripheral ring enhancement is signifying tuberculoma

Disseminated tuberculosis in a pregnant woman presenting with numerous brain tuberculomas:49

Inflammatory disordersIn systemic lupus erythematosus cerebral calcifications have been seen in the basal ganglia, centrum semiovale, cerebellum and thalamusNeurosarcoidosis.Lesions involve the parenchyma, leptomeninges and dura mater.The hallmark of neurosarcoidosis is the basal leptomeningeal involvement

TumorsNeoplastic calcifications usually suggest a more benign processmeningioma craniopharyngiomachoroid plexus papillomaependymomaglioma (especially oligodendroglioma, also astrocytoma)gangliogliomalipoma of corpus callosumpinealomahamartoma of tuber cinerium

TumorsMetastasis.Intracranial calcification may occur from lung, breast, colon cancer and osteogenic sarcoma.

Massive calcifications in right frontal lobe colon cancer metastasis52

Oligodendroglioma: is the most common intracranial neoplasm associated with calcifications. The calcifications can be central or peripheral, punctate or ribbon-like, located within walls of intrinsic tumor vessels, and they may extend to the surrounding brain parenchyma.

Cystic component may be present and the enhancementis variable

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Subcortical/cortical large left frontal oligodendroglioma (a) NECT, (b) MRI withGd - heterogenous mass with nodular calcification (arrows) and cystic component (star)54

Astrocytoma: In diffuse low grade astrocytoma calcification are described as linear, punctate or multifocal, diffuse and may follow the white-matter tracts (more often in large tumors).Up to 20-25% of pilocytic astrocytomas have intratumoral calcification

Calcified chunks or nodules are present in most of the subependymal giantcell astrocytomas and may be associate with other finding of tuberous sclerosis55

Ependymoma:magna and cerebellopontine angle;calcifications (~50% of cases) ranging from small punctate foci to large masses; associated with hydrocephalus

# presents as irregular shape mass in the 4th ventricle, extending in cisterna

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Craniopharyngioma.partially calcified, partial solid, cystic suprasellar mass in children,sometimes is associated with circle of Willis displacement.

Obstructive craniofaringioma. Axial NECT (a)- Heterogenous supraselarmasse with periferal calcification (red arrows) and hipodens area; hydrochephalyassociated(star); (b) CECT - Little enhancement (small white arrows) and milddisplcement of Circle of Willis (large white arrow).58

Meningiomas About 25-30% of meningiomas are fully calcified on CT.

The calcifications are either focal or diffuse, psammomatous, rim or have radial pattern.

Locations: 85 - 90% supratentorial, infratentorial or miscellaneous. CT features: extra-axial lesion ("inward buckling"); isodense or hyperattenuating to parenchyma; underlying parenchymal edema; homogeneous and vigorously enhancement "dural tail" sign; hyperostosis or osseous erosion

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Large left paraselar meningioma. (a) NECT heterogenous mass with diffusecalcification, (b) MRI with Gd- homogenous enhancement (white arrow).60

Causes of basal ganglia calcification

Metabolic related: Hypothyroidism may exhibit calcification in basal ganglia and cerebellum. Hypoparathyroidism, either idiopathic or following thyroidectomy, is the most important cause. Calcification involve the basal ganglia, the thalamus and the cerebellum.

Hypoparathyroidism, either idiopathic or following thyroidectomy, is the most important cause because it may be treatable. Calcification involve the basal ganglia, the thalamus and the cerebellum.

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Hyperparathyroidism is associated with subcortical and basal ganglia calcification.Lead toxicity intracranial calcification are common confined to globus pallidus

Fahr disease, also known as bilateral striopallidodentate calcinosis, showing characteristic calcification in lateral globus pallidus.Hallervorden Spatz disease is a neurodegenerative disease with hyperintensity in globus pallidus represented by brain iron accumulation.

Others causes:

-Ischemic:carbon monoxide intoxication, birth anoxia (generally limited to globus pallidus)Congenital:trisomy 21Chemotherapy:methotrexate

Radiation therapy In post radiation therapy calcifications are commonly found in subcortical white-matter and basal ganglia in mineralizing microangiopathy and in posterior white-matter areas in necrotizing leukoencephalopathy.

Mineralizing microangiopathy. Small bilateral calcifications involving thethalamo-lenticular regions and the subcortical white matter (arrows).66

Miscellaneous

hematoma: ICH, EDH or SDH. Calcifications usually only when chronic

idiopathic

Conclusion1.Intracranial calcifications are relatively common and CT is the most sensitive method in their detection and proper location.2.The presence of intracranial calcifications, their distribution and semiologcal appearance in association with the clinic and biological data and in particular cases the follow up of the patient, help to make an accurate diagnosis.

MERCI

referencesMathias Prokop - Computed Tomography of the Body [1]. Greenberg H, Chandler WF, Sandler HM. Brain tumors. Oxford University Press, USA. (1999) ISBN:019512958X.K#ro#lu Y, Call# C, Karabulut N et-al.Bennett Greenspan, MD Instructor of Radiology, Mallinckrodt Institute of Radiology, Washington University School of Medicine , Tuberous Sclerosis Imaging - Intracranial calcifications on CT. DiagnIntervRadiol.2010.EriniMakariou, MD, and Athos D. Patsalides, MD-Intracranial calcifications.Neuroradiology Unit, S P Institute of Neurosciences,Solapur,Maharashtra, INDIAMarkS. Greenberg Handbook of Neurosurgery Seventh edition