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Intracranial calcifications on CT
Yılmaz Kıroğlu1, Cem Çallı3, Nevzat Karabulut1, Çağatay Öncel2
1From the Departments of Radiology, Pamukkale University Faculty of Medicine, Denizli, Turkey
2From the Departments of Neurology, Pamukkale University Faculty of Medicine, Denizli, Turkey
3Department of Radiology, Ege University Faculty of Medicine, İzmir, Turkey
Keywords: • calcification, physiologic • calcification, pathologic• computed tomography
DOI: 10.4261/1305-3825.DIR.2626-09.1
Summary
Computed tomography (CT) is very sensitive for detection and localization of intracranial calcifications. We reviewed in this pictorial essay the diseases associated with intracranial calcifications and emphasized the utility of CT for the differential diagnosis.
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  • Summary
  • Introduction
  • References
  • Introduction
    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 (


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    Table
    ).


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    Table: . Intracranial calcifications

    Age-related physiologic and neurodegenerative calcifications
    Intracranial physiologic calcifications are unaccompanied by any evidence of disease and have no demonstrable pathological cause[1]. The most common sites include the pineal gland, habenula, choroid plexus, basal ganglia, falx, tentorium, petroclinoid ligaments and sagittal sinus. Calcification of the pineal gland is seen 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[2]. Habenula 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. Choroid plexus calcification is very common finding, usually in the atrial portions of the lateral ventricles (Fig. 1). Calcification in the third or fourth ventricle or in patients less than 9 years of age is uncommon. Basal ganglia calcifications are usually idiopathic incidental findings that have a 0.3–1.5% incidence and increases with age. They usually demonstrate a faint punctuate or a coarse conglomerated symmetrical calcification pattern[1] (Fig. 2). 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 cerebrum[2] (Fig. 3). Dural and tentorial calcifications are usually seen in a laminar pattern and can occur anywhere within the cranium (Fig. 4). Petroclinoid ligament and sagittal sinus calcifications are common age-related degeneration sites and usually have laminar or mildly nodular patterns[1,2] (Fig. 5).


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    Figure 1: Bilateral choroid plexus (arrowheads), pineal (arrow) and habenular calcifications (dashed arrow) on axial CT.


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    Figure 2: Calcifications in bilateral basal ganglia.


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    Figure 3: Calcified falx cerebri on the anteroposterior axis.


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    Figure 4: Calcifications along the tentorium cerebelli.


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    Figure 5: Calcified bilateral petroclinoid ligaments (arrows).

    Congenital calcifications
    This condition is frequently seen in Sturge-Weber syndrome (SWS), tuberous sclerosis (TS) and intracranial lipoma, but rarely in neurofibromatosis (NF), Cockayne (CS) and Gorlin syndromes (GS). SWS is a rare disorder consisting of a port-wine nevus in the distribution of the ophthalmic branch of the trigeminal nerve and nervous system malformations. The syndrome results from malformation of the cerebral vasculature located within the pia mater. This malformation leads to venous hypertension and subsequent hypoperfusion of the underlying cortex, causing chronic cerebral ischemia, parenchymal atrophy, enlargement of the ipsilateral choroid plexus and calcification. Calcification in SWS demonstrates a characteristic linear cortical pattern[3] (Fig. 6). TS is an autosomal dominant disorder characterized by mental retardation, epilepsy and adenoma sebaceum. Intracranial lesions in TS consist of subependymal hamartomas, subcortical tubers, giant cell tumors, and white matter lesions. Calcifications of the subependymal nodules are pathognomonic and commonly located along the caudothalamic groove and atrium. Subcortical tubers are calcified more often in elderly patients[4] (Fig. 7). NF1 is an autosomal dominant disorder characterized by gliomas, dysplasias and hamartomas. Intracranial hamartomas in NF1 are frequently seen in the location of globus pallidus, but they rarely calcify[5]. Intracranial lipomas are benign congenital malformations, which progress asymptomatically. Approximately 80–90% of intracranial lipomas are located at or near the midline. A curvilinear or focal pattern of calcifications is frequently seen in their capsules and surrounding parenchyma[6] (Fig. 8). CS is an autosomal recessive disorder, which shows progressive encephalopathy including intracranial calcifications and white matter lesions. Calcifications are commonly in coarse pattern and frequently involve the subcortical white matter, basal ganglia and dentate nuclei. GS is an autosomal dominant tumor predisposition syndrome that consists of multiple basal cell carcinomas of the skin, odontogenic keratocyst of the jaw, various skeletal abnormalities, and lamellar falx calcification[7] (Fig. 9).


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    Figure 6: Characteristic gyral calcifications in Sturge-Weber syndrome associated with atrophy of the right frontal and temporal lobes.


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    Figure 7: a, b. Periventricular calcifications of subependymal nodules in two different patients with tuberous sclerosis. Subcortical calcified tuber (arrow) in the right parietal lobe (a).


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    Figure 8: Intracranial lipoma in the midline of cerebrum with thin focal calcifications (arrows).


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    Figure 9: a, b. Dentigerous keratocysts in both sides of the jaw (a) and midline falcian calcification (b) in Gorlin’s syndrome.

    Infectious calcifications
    A large number of infectious agents may involve the fetal central nervous system in utero. The most common of them are ’’TORCH’’ agents including toxoplasmosis, rubella, Cytomegalovirus (CMV) and Herpes simplex virus (HSV). Congenital HSV infections demonstrate extensive cerebral destruction, multicystic encephalomacia and scattered calcifications[8]. Congenital toxoplasmosis is commonly associated with hydrocephalus and randomly nodular calcifications in periventricular, basal ganglia and cerebral cortical areas (Fig. 10). Congenital rubella is usually associated with meningitis, ventriculitis and subsequent ventriculomegaly. Calcifications are commonly located in the periventricular white matter, basal ganglia, and brain stem[9]. CMV is the most common cause of congenital infections and frequently associated with microcephaly, chorioretinitis, and intracranial calcifications. Calcifications in congenital CMV infections are commonly seen in the periventricular and subependymal sites[8] (Fig. 11).


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    Figure 10: Axial unenhanced CT shows extensive bilateral thalamic and periventricular calcifications associated with dilated ventricular asymmetry in congenital toxoplasmosis.


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    Figure 11: Extensive periventricular and subependimal calcifications with marked hydrocephaly in congenital Cytomegalovirus infection.

    Chronic phase of viral encephalitis may feature widespread encephalomalacia and calcification in the residual parenchyma as a rare infectious cause of intracranial calcifications[9].

    Calcification in intracranial tuberculosis and fungal opportunistic granulomatous infections is also quite rare. A ‘’target sign’’ representing a central nidus of calcification surrounded by a ring of enhancement is strongly suggestive of a tuberculoma[8,10]. Although subdural and epidural empyemas are common complications of intracranial infections, they may rarely demonstrate calcified meninges and low density effusions in the chronic phase of the illness (Fig. 12).


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    Figure 12: Unenhanced CT image shows low-density epidural effusions with calcified walls (arrows) adjacent to the right parietal lobe.

    Calcifications related with hormonal and metabolic disorders
    Fahr disease is a rare degenerative neurological disorder characterized by extensive bilateral basal ganglia calcifications that can lead to progressive dystonia, parkinsonism and neuropsychiatric manifestations. It is associated with defective iron transport resulting in tissue damage with extensive calcification. Metastatic deposition is frequently located in the bilateral basal ganglia, dentate nuclei, cerebral white matter, and internal capsule[11] (Fig. 13). Fahr patients are usually asymptomatic in the first two decades of life, despite the presence of intracranial calcifications.


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    Figure 13: a, b. Dense calcifications in the bilateral corpora striatum and thalami (a), and in the cerebellar parenchyma (b) associated with Fahr disease.

    Function of the parathyroid hormone is primarily maintaining the plasma calcium levels. Hormonal disturbance of the parathyroid glands including hypoparathyroidism, hyperparathyroidism and pseudohypoparathyroidism may lead to intracranial calcifications. Calcium accumulation is demonstrated primarily in the bilateral basal ganglia, dentate nuclei, and peripheral subcortical white matter sites[12] (Fig. 14).


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    Figure 14: a, b. Extensive calcifications in the bilateral corpora striatum and peripheral cerebral subcortical areas (a), dentate nuclei and cerebellar parenchyma (b) associated with hypoparathyroidism.

    Vascular calcifications
    Calcification of the intracranial arteries associated with primary atherosclerosis is more frequent in elderly people. The highest prevalence of intracranial artery calcification is seen in the internal carotid artery (60%), followed by the vertebral artery (20%), middle cerebral artery (5%), and basilar artery (5%)[13] (Fig. 15).


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    Figure 15: a–c. Primary atherosclerotic calcified plaques are demonstrated on the walls of the internal carotid (a) and bilateral vertebral arteries (arrows) (b, c).

    Other causes of vascular calcifications include aneurysm, arteriovenous malformation (AVM) and cavernous malformation. Although patent aneurysms may contain mural calcification, partially or completely thrombosed aneurysms commonly have calcifications[14] (Fig. 16). AVMs may contain dystrophic calcifications along the serpentine vessels and within the adjacent parenchyma with a prevalence of 25–30%[13] (Fig. 17). Cavernous malformation is a benign vascular hamartoma that is frequently calcified in a ’’popcorn-ball’’ fashion[15] (Fig. 18).


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    Figure 16: Unenhanced axial CT scan shows a giant aneurysm with a rimlike calcified wall arising from the anterior communicating artery (arrow). Calcification in the right middle cerebral artery walls (arrowhead), surrounding edema, and hydrocephalus with intraventricular hemorrhage (dashed arrow) are also seen.


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    Figure 17: a, b. Extensive serpentine calcifications in the parietooccipital cerebral parenchyma and left choroid plexus extend from the deep periventricular region towards the cortex with accompanying atrophy in a large arteriovenous malformation.


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    Figure 18: Cavernous malformation in a ”popcorn-ball” appearance with a thick and dense rim calcification pattern in the right parietal lobe.

    Neoplastic calcifications
    The most common intracranial neoplasms associated with calcifications[16] are oligodendroglioma (70–90%), craniopharyngioma (50–80%), germ cell neoplasms (dysgerminoma, seminoma, teratoma, choriocarcinoma; 60–80%), pineal neoplasms (pineoblastoma, pineocytoma; 60–80%), central neurocytoma (50–70%), primitive neuroectodermal tumor (PNET) (50–70%), ependymoma (50%), ganglioglioma (35–50%) (Fig. 19), dysembriyonic neuroectodermal tumor (DNET) (20–36%), meningioma (20–25%), choroid plexus papilloma (25%), medulloblastoma (20%), low grade astrocytoma (20%), and pilocytic astrocytoma (10%). Calcifications are rarely seen in schwannomas, and dermoid and epidermoid tumors.


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    Figure 19: Ganglioglioma in the right temporal lobe as a partially cystic, cortexbased mass with nodular calcification (arrow).

    Evaluation of neoplastic calcifications along with the patient age, tumor localization and calcification pattern may contribute to the radiologic differential diagnosis of intracranial neoplasms. Oligodendrogliomas are usually located in the frontal lobe and are calcified in a nodular and clumped pattern (Fig. 20). Craniopharyngioma is characterized by a suprasellar mass that is calcified in an amorphous and lobulated pattern (Fig. 21). A dural based tumor in an elderly patient, with a variable pattern of calcifications including diffuse, focal, sandlike, sunburst, and globular, strongly suggests a meningioma[17] (Fig. 22). A cortexbased cystic mass with a mural calcific nodule in a young patient may suggest a ganglioglioma. A heterogenous, calcified mass in the pineal region in a young patient may suggest a germ cell neoplasia (Fig. 23). Calcifications are fairly rare in metastases with the exceptions of osteogenic sarcoma and mucinous adenocarcinoma. Metastases treated by radiotherapy or chemotherapy may also develop calcification[2].


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    Figure 20: a, b. Oligodendrogliomas in two different cases. First is in the right frontal lobe and represents a partially calcified cortexbased mass (a) while the second is located in the left periventricular area (b). Calcifications of both masses are in a nodular and clumped pattern.

    Figure 21: a, b. Craniopharyngiomas in two different patients in sellar and suprasellar regions with amorphous calcifications.

    Figure 22: Bone-window unenhanced CT image demonstrates a meningioma as a dural-based cortical mass with dense globular calcification in the left frontal lobe.

    Figure 23: Teratoma in a newborn patient in the right cerebral hemisphere with coarse anterior calcifications.

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  • Summary
  • Introduction
  • References
  • References
    1) Kieffer SA, Gold LH. Intracranial physiologic calcifications. Semin Roentgenol 1974; 2:151–162.

    2) Deepak S, Jayakumar B. Intracranial calcifications. J Assos Physicians India 2005; 53:948.

    3) Wasenco JJ, Rosenbloom SA, Duchesneau PM, Lanzieri CF, Weinstein MA. The Sturge-Weber syndrome: comparison of MR and CT characteristic. AJNR Am J Neuroradiol 1990; 1:131–134.

    4) Lin DD, Barker PB. Neuroimaging of phakomatoses. Semin Pediatr Neurol 2006; 1:48–62.

    5) Arts WF, Van Dongen KJ. Intracranial calcified deposits in neurofibromatosis. J Neurol Neurosurg Psychiatry 1986; 11:1317–1320.

    6) Yilmaz N, Unal O, Kiymaz N, Yilmaz C, Etlik O. Intracranial lipomas. Clin Neurol Neurosurg 2006; 4:363–368.

    7) Kantarci M, Ertas U, Sutbeyaz Y, Karasen RM, Onbas O. Gorlin’s syndrome with a thin corpus callosum and a third ventricular cyst. Neuroradiology 2003; 6:390–392.

    8) Sze G, Lee SH. Infectious disease. In: Lee SH. Rao KCVG, Zimmerman RA, eds. Cranial MRI and CT. 4th ed. New York: Mc Graw-Hill, 1999; 453–517.

    9) Hedlung GL, Boyer RS. Neuroimaging of postnatal pediatric central nervous system infections. Semin Pediatr Neurol 1999; 4:299–317.

    10) Alkan A, Parlak M, Baysal T, Sigirci A, Kutlu R, Altinok T. En-plaque tuberculomas of tentorium in a pregnant women: follow-up with MRI. Eur Radiol 2003; 5:1190–1193.

    11) Acou M, Vanslembrouck J, Deblaere K, Bauters W, Achten E. Fahr disease. JBR-BTR 2008; 1:19.

    12) You JS, Kim HJ, Chung SP, Park S. Intracranial bilateral symmetric calcification in hypoparathyroidism. Emerg Med J 2008; 3:162.

    13) Chen XY, Lam WW, Ng HK, Fan YH, Wong KS.The frequency and determinants of calcification in intracranial arteries in Chinese patients who underwent computed tomography examinations. Cerebrovasc Dis 2006; 21:91–97.

    14) Tomandl BF, Köstner NC, Schempershofe M, Huk WJ, Strauss C, Anker L, Hastreiter P. CT angiography of intracranial aneurysms: a focus on post processing. Radiographics 2004; 3:637–655.

    15) Metoki T, Mugikura S, Higano S, Ezura M, Matsumoto Y, Hirayama K, Takahashi S. Subcortical calcification on CT in dural arteriovenous fistula with cortical venous reflux. AJNR Am J Neuroradiol 2006; 5:1076–1078.

    16) Rabinov JD. Diagnostic imaging of angiographically occult vascular malformations. Neurosurg Clin N Am 1999; 3:419–432.

    17) Rees J, Lee SH, Smirniotopoulos JG. Primary brain tumors in adults. In: Lee SH. Rao KCVG, Zimmerman RA, eds. Cranial MRI and CT. 4th ed. New York: Mc Graw- Hill, 1999: 261–341.
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  • Summary
  • Introduction
  • References