|Article Type:||Clinical report|
CT imaging (Health aspects)
Calcification (Physiological aspects)
Central nervous system diseases (Risk factors)
Central nervous system diseases (Diagnosis)
Central nervous system diseases (Care and treatment)
Central nervous system diseases (Patient outcomes)
Patsalides, Athos D.
|Publication:||Name: Applied Radiology Publisher: Anderson Publishing Ltd. Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2009 Anderson Publishing Ltd. ISSN: 0160-9963|
|Issue:||Date: Nov, 2009 Source Volume: 38 Source Issue: 11|
|Topic:||Event Code: 310 Science & research|
|Geographic:||Geographic Scope: United States Geographic Code: 1USA United States|
Intracranial calcifications seen on computed tomography (CT) are
the most common finding in the everyday practice of neuroradiology,
because noncontrast-enhanced CT of the head is the preferred imaging
modality worldwide for the initial evaluation of patients with acute or
chronic neurological problems. The intracranial calcifications may have
no clinical importance or they may be critical findings in diagnosing
the underlying pathology.
In this article, we illustrate a broad spectrum of common and uncommon central nervous system (CNS) disorders associated with calcifications. In order to provide a systematic review and an approach to a more accurate diagnosis, we present the intracranial calcifications according to the underlying etiology. The neoplastic processes are subdivided according to location (Table 1).
The physiologic calcifications are very common and have been well-described in the past decades. They are associated with aging and can be seen in the basal ganglia, pineal gland, falx, tentorium, arachnoid granulations, choroid plexus and the cerebellum. Physiologic calcifications are almost never clinically significant. The calcifications in the basal ganglia are usually punctate and are located within the globus pallidus, the head of the caudate nucleus, and the putamen and are very common in middle-aged individuals and the elderly (Figure 1). However, basal-ganglia calcifications in persons <30 years of age can be associated with underlying metabolic disorders, such as hyper- or hypoparathyroidism, congenital disorders such as Fahr disease, and infections. The presence of basal-ganglia calcifications in patients <30 years of age should prompt careful clinical evaluation to rule out another etiology (Table 2). Physiologic calcifications of the pineal gland (Figure 2) are seen in approximately 40% of normal people by the age of 20 years (1) and appear compact, measuring <1 cm in diameter. Larger calcifications should raise concerns for underlying tumor, as discussed later in this article.
The habenular commisure, anterior to the pineal gland, is another location for physiologic calcifications. Physiologic calcifications of the dura (Figure 3) are also very common in older age groups and are usually located in the falx or the tentorium. Presence of dural calcifications in children should raise the suspicion of underlying pathology, mainly basal-cell nevus syndrome.
Arachnoid granulations, especially large ones within the transverse and sigmoid sinuses, are also calcified in middle-aged and older people with characteristic appearances. (2) The physiologic calcifications of the choroid plexus (Figure 2) are very common after the age of 40 years. On the other hand, only 2% of children between 0 to 8 years of age and 9.5% of children from 9 to 15 years of age have calcifications of the choroids plexus. (3)
Finally, physiologic calcifications can be seen in the cerebellum, with the dentate nucleus (Figure 4) being the most common site. (4)
The dystrophic calcifications are chronic sequelae of trauma, surgery, ischemia and radiation therapy. Parenchymal dystrophic calcifications are often associated with encephalomalacia and reactive gliosis.
Posttraumatic calcifications have been described in the capsule surrounding both chronic subdural (Figure 5) (5) and epidural hematomas. (6) This finding is more common in chronic subdural hematomas, seen in 1% to 2% of patients. Isolated case reports have presented rapidly calcified epidural hematomas. (7) Radiation therapy and, to a lesser extent, chemotherapy have been implicated in the appearance of significant detrimental effects on the CNS. Because of the slow replication rate of most constituents of the CNS, these effects tend to be delayed. Radiation-therapy- and chemotherapy-related calcifications are much more common in young children. (8) Three main types of calcifications have been observed:
* necrotizing leukoencephalopathy, which results in white-matter calcifications in the posterior hemisphere; and,
* dystrophic brain calcifications.
Although radiation therapy and chemotherapy probably have a synergistic role in the pathogenesis, radiation is the dominant factor in mineralizing microangiopathy. Finally, ischemic and hemorrhagic infarcts, parenchymal hemorrhage from trauma, and prior surgery are also associated with dystrophic calcifications.
The phakomatoses are a group of hereditary disorders that affect structures of ectodermal origin. Classically, calcifications are described in tuberous sclerosis and Sturge-Weber syndrome but can also be seen in neurofibromatosis and basal-cell nevus syndrome.
Calcified subependymal hamartomas are common findings in tuberous sclerosis, usually located along the ventricular surface of the caudate nucleus (Figure 6), just posterior to the foramen of Monro. The cortical hamartomas seen in tuberous sclerosis are usually supratentorial and can also calcify. Calcifications in the subependymal and cortical hamartomas are rare during the first year of life and the rate increases along with the patient's age.
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
[FIGURE 3 OMITTED]
[FIGURE 4 OMITTED]
[FIGURE 5 OMITTED]
[FIGURE 6 OMITTED]
Subependymal giant-cell astrocytomas are another major manifestation of tuberous sclerosis that can present as a calcified nodule. These lesions are larger than the subependymal nodules, show interval growth, enhance on post-contrast images and are located at or near the foramen of Monro. (9) Gyriform cortical calcifications, with a pattern similar to Sturge-Weber, are sometimes seen as well. (10)
The most common calcifications seen in patients with neurofibromatosis type 2 (NF2) are the ones associated with disease-related tumors, such as meningiomas. Nontumoral calcifications have also been described in these patients, with symmetric or asymmetric calcifications of the choroid plexus in the lateral ventricles and nodular calcifications of the cerebellum (11) being most commonly observed. Cortical calcifications are less common. Vouge et al. (12) described subependymal calcifications in a series of patients with NF2, similar to the calcifications seen in tuberous sclerosis.
[FIGURE 7 OMITTED]
[FIGURE 8 OMITTED]
[FIGURE 9 OMITTED]
[FIGURE 10 OMITTED]
Early dural calcifications are a common manifestation of the basal-cell nevus syndrome; they involve the falx (Figure 7), the diaphragma sella and the tentorium. These are also locations of physiologic calcifications, but in patients with basal-cell nevus syndrome, the calcifications appear in younger age groups. (13) One of the typical imaging findings in Sturge-Weber syndrome is calcification occurring adjacent to a pial angioma, originating in the subcortical white matter and then extending to the cortex (Figure 8). The parieto-occipital cortex is the most common location for cortical calcifications, but they may occur anywhere in the cerebrum. In 20% of patients these calcifications are bilateral. (14)
Calcifications in the arterial wall of large intracranial vessels are common and should be mentioned in the report because of their association with atherosclerosis. It is also important to be aware of other calcification patterns associated with vascular pathology, such as vascular malformations and aneurysms.
Atherosclerosis is associated with mural calcifications of the major intracranial arteries. (15) The carotid siphon (Figure 9) is the most commonly affected vessel, while calcifications in the anterior and middle cerebral arteries and the vertebrobasilar system (Figure 10) are less common.
Arteriovenous malformations (AVMs) are associated with dystrophic intracranial calcifications. These are seen in the watershed or other areas away from the AVM nidus due to ischemic brain tissue as a result of the "vascular steal" from the AVM. (16) Calcification can also be seen in the AVM nidus. (17) AVMs are associated with mural calcifications in the ectatic veins associated with the fistula. (18) Patients with cavernous angiomas (Figure 11) often have stippled calcifications (19) in the vessel wall or the adjacent brain parenchyma.
These are more commonly seen in nonhemorrhagic lesions. (20) Calcifications in developmental venous anomalies (venous angioma, Figure 12) and capillary telangiectasias have been occasionally described. (21-23) Brain aneurysms (Figure 13) often have mural calcifications, more often seen in fusiform (24) compared with saccular aneurysms. Amyloid angiopathy results in gyriform calcification and sclerotic changes in the medullary arteries. (25)
[FIGURE 11 OMITTED]
[FIGURE 12 OMITTED]
[FIGURE 13 OMITTED]
Intracranial calcifications are common in patients with congenital infections, but their appearance is not specific because they reflect dystrophic calcifications similar to any chronic brain injury. Basal ganglia and cortical calcifications are common features of all infections that constitute the TORCH syndrome (toxoplasmosis, other, rubella, cytomegalovirus, herpes simplex virus).
Cytomegalovirus and toxoplasmosis (Figure 14) infections result in periventricular and subependymal calcifications. (26) Interestingly, calcifications in patients infected with toxoplasmosis may resolve after treatment. (27) Congenital HIV infection (Figure 15) is associated with periventricular frontal white-matter and cerebellar calcifications. (28) Congenital herpes (HSV-2) infection is associated with thalamic, periventricular, and punctate cortical (29) or extensive gyral calcifications. (30)
[FIGURE 14 OMITTED]
Cysticercosis, tuberculosis, HIV and cryptococcus are the most common acquired intracranial infections typically associated with calcifications. As in the case of congenital infections, the pattern of calcification is not specific but is still useful in making the diagnosis and evaluating disease progression.
In cysticercosis (Figure 16), calcifications are seen in the dead larva (granular-nodular stage) and the typical appearance is that of a small, calcified cyst containing an eccentric calcified nodule that represents the dead scolex. The most common locations for the calcifications are the subaracnhoid spaces in the convexities, ventricles, and basal cisterns and the brain parenchyma, especially the gray-white matter junction.
Tuberculosis results in calcified parenchymal granulomata in 10% to 20% of patients; (31) meningeal calcifications are much less common. HIV encephalitis is associated with basal ganglia calcification. (32) Cryptococcus affects immunocompromised patients and calcifications can be seen in both the brain parenchyma (33) and the leptomeninges. (34)
[FIGURE 15 OMITTED]
Sarcoidosis involves the leptomeninges, producing granulomas of the pituitary stalk and the optic chiasm. Calcified sarcoid granulomas can also be seen in the pituitary, pons, hypothalamus and the periventricular white matter. Systemic lupus erythematosus (Figure 17) has been associated with cerebral calcifications in the basal ganglia, thalamus, cerebellum and centrum semiovale. (35)
Commonly calcified intracranial tumors include the oligodendrogliomas, low-grade astrocytomas, craniopharyngiomas, meningiomas, pineal gland tumors and the ependymomas. Since many tumors have overlapping imaging findings, knowing which tumors calcify is useful in limiting the differential diagnosis. In some instances, the presence and pattern of calcification can be essentially pathognomonic as in the case of oligodendrogliomas and craniopharyngiomas.
We present the intracranial tumors that calcify divided into intra- and extra-axial and intraventricular, in order to make the differential diagnosis more meaningful. The presence or absence of calcifications is not related to the benign or malignant nature of the tumor.
The diffuse low-grade astrocytomas (Figure 18) are the most common glial neoplasms demonstrating calcifications; however, only the minority of these tumors calcify. (36) The calcification can be linear, diffuse, punctate or multifocal and may follow the white-matter tracts, especially with large tumors. (37) Calcifications are present in the majority of subependymal giant-cell astrocytomas in the form of calcified chunks or nodules. (38,39) Up to 25% of pilocytic astrocytomas have intratumoral calcification. Other astrocytomas such as the pleomorphic xanthostrocytoma, anaplastic astrocytomas and glioblastoma multiforme (Figure 19) only rarely calcify.
[FIGURE 16 OMITTED]
The oligodendrogliomas (Figure 20) exhibit the highest frequency of calcification among all brain tumors, since up to 90% of them calcify. (40,41) The calcifications in oligodendrogliomas can be central or peripheral, punctate or ribbon like, usually located within walls of intrinsic tumor vessels. (42) Calcifications may even extend to the surrounding brain parenchyma. The medulloblastomas show small, clumplike or nodular calcifications in approximately 20% of cases. (43) Calcifications are typically seen in the majority of gangliocytomas (44) and in approximately 40% of gangliogliomas (Figure 21). (45) The calcifications are more commonly seen in cystic rather than solid gangliogliomas. (46) Dysembryoplastic neuroepithelial tumors have a calcification pattern similar to oligodendrogliomas but only a small percentage of these tumors calcify. (47) Calcified intracranial metastases (Figure 22) are very rare and have been primarily described in case reports. (48) The osteogenic sarcoma, lung and breast carcinomas are the most common primary tumors with brain metastases that calcify. (49)
[FIGURE 17 OMITTED]
The percentage of meningiomas (Figures 23-25) that calcify ranges from 20% to 69%. (36,50) The calcifications can be focal, diffuse, coarse, sand-like or even rim. There is a higher percentage of calcified meningiomas in children, which could be associated with more aggressive subtypes of meningiomas. (51) Pineal gland calcifications are very common: seen in approximately 40% of normal people by the age of 20 years. (1) Compact pineal calcifications measuring <1 cm in diameter are not associated with underlying pathology. Larger pineal gland calcifications however, are worrisome for pineal gland tumors.
[FIGURE 18 OMITTED]
[FIGURE 19 OMITTED]
[FIGURE 20 OMITTED]
[FIGURE 21 OMITTED]
[FIGURE 22 OMITTED]
Among the pineal cell parenchymal tumors, the pineocytomas are the ones that calcify more frequently, showing either peripheral or central calcifications. Peripheral calcifications are thought to be native pineal body calcifications displaced by the tumor, whereas the central calcifications are produced by the tumor itself. (52) Among the pineal tumors arising from germ cells, teratomas commonly have dense calcifications. The germinomas very rarely calcify but may displace or engulf preexisting physiologic pineal gland calcifications. (53) Seventy percent to ninety percent of craniopharyngiomas (Figure 26) are seen in children with calcifications, and 30% to 40% of craniopharyngiomas are seen in adults who have calcifications. This is explained by the different histology of the tumor in different age groups; the adamantinous craniopharyngiomas are usually seen in children and almost always (90%) calcify either in the periphery and/or the solid component of the tumor. (54) The squamous papillary craniopharyngiomas are more often seen in adults and are less likely to calcify. Dermoid and epidermoid tumors show peripheral stippled calcification in approximately 20% to 25% of cases (55) while teratomas typically show internal calcifications. (56) Pituitary adenomas do not calcify frequently. They should be suspected however, when calcification is seen within the pituitary gland. (57,58)
[FIGURE 23 OMITTED]
[FIGURE 24 OMITTED]
[FIGURE 25 OMITTED]
Pericallosal and interhemispheric lipomas may show calcification of the fibrous capsule with rim or eggshell appearance. The calcification can also be located in the center of the lipoma. Lipomas located elsewhere, are much less likely to show calcifications. (59,60) Colloid cysts rarely calcify. (61)
Intraventricular ependymomas typically calcify, ranging from punctate to mass-like calcifications. (62,63) Posterior fossa ependymomas exhibit small, round calcifications up to 50% (64) and have the highest frequency of calcification among the posterior fossa tumors. The subependymomas calcify in approximately one third of cases and usually demonstrate small foci of calcification. (65,66) The choroid plexus papillomas and carcinomas have punctate calcifications in approximately 25% of cases. (38) The central neurocytomas (Figure 27) were thought to characteristically show globular calcifications. (68) Other authors, however, reported calcifications in only 50% of these tumors. (67) The calcification in these tumors is variable, ranging from punctate to mass like. Intraventricular meningiomas (Figure 28) calcify in approximately 50% of cases, (62) with calcification patterns similar to the extraaxial meningiomas.
[FIGURE 26 OMITTED]
[FIGURE 27 OMITTED]
[FIGURE 28 OMITTED]
[FIGURE 29 OMITTED]
Metabolic disorders affecting the calcium homeostasis are associated with intracranial calcifications that predominantly involve the basal ganglia. Although the pattern is similar to the physiologic, age-related calcifications, they appear at younger ages and are often progressive. Basal ganglia and subcortical calcifications have been described in patients with chronic renal failure and secondary hyperparathyroidism (Figure 29). (69) In patients with hypoparathyroidism (Figure 30), the calcifications typically involve the basal ganglia, thalami, and the cerebellum. (70) Intracranial calcifications are more commonly seen in the pseudorather than idiopathic hypoparathyroidism. (71) Hypothyroidism is also associated with basal ganglia and cerebellar calcifications.
[FIGURE 30 OMITTED]
Intracranial calcifications can also be seen in rare idiopathic disorders such as Fahr disease (bilateral striopallidodentate calcinosis, Figure 31). This disease shows characteristic calcifications in the basal ganglia, especially in the lateral globus pallidus. Other involved areas are the thalami, the cerebral white matter and the dentate nuclei of the cerebellum. (72) Progressive and symmetric basal ganglia calcifications are the commonest radiological finding of MELAS syndrome. (73)
Knowledge of physiologic calcifications in the brain parenchyma is essential to avoid misinterpretations. However, several pathologic conditions involving the brain are associated with calcifications and the recognition of their appearance and distribution helps narrow the differential diagnosis.
[FIGURE 31 OMITTED]
(1.) Zimmerman RA, Bilaniuk LT. Age-related incidence of pineal calcification detected by computed tomography. Radiology. 1982;142:659-662.
(2.) Roche J, Warner D. Arachnoid granulations in the transverse and sigmoid sinuses CT, MR, and MR angiographic appearance of a normal anatomic variation. AJNR Am J Neuroradiol. 1996;17:677-683.
(3.) Kendall B, Cavanagh N. Intracranial calcification in paediatric computed tomography. Neuroradiology. 1986;28:324-330.
(4.) Koller WC, Klawans HL. Cerebellar calcification on computerized tomography. Ann Neurol. 1980;7: 193-194.
(5.) Sato K, Yamada M, Shimzu S, et al. Infected and calcified chronic subdural hematoma presenting an attitude of acute hematoma on MRI: Case report. No Shinkei Geka. 2005;33:805-808.
(6.) Chang JH, Choi JY, Chang JW, et al. Chronic epidural hematoma with rapid ossification. Childs Nerv Syst. 2002;18:712-716.
(7.) Erdogan B, Sen O, Bal N, Cekinmez M, et al. Rapidly calcifying and ossifying epidural hematoma. Pediatr Neurosurg. 2003;39:208-211.
(8.) Fernandez-Bouzas A, Ramirez Jimenez H, Vazquez Zamudio J, et al. Brain calcifications and dementia in children treated with radiotherapy and intrathecal methotrexate. J Neurosurg Sci. 1992;36: 211-214.
(9.) Kingsley DP, Kendall BE, Fitz CR. Tuberous sclerosis: A clinicoradiological evaluation of 110 cases with particular reference to atypical presentation. Neuroradiology. 1986;28:38-46.
(10.) Wilms G, Van Wijck E, Demaerel P, et al. Gyriform calcifications in tuberous sclerosis simulating the appearance of Sturge-Weber disease. AJNR Am J Neuroradiol. 1992;13:295-7.
(11.) Mayfrank L, Mohadjer M, Wullich B. Intracranial calcified deposits in neurofibromatosis type 2. A CT study of 11 cases. Neuroradiology. 1990;32:33-37.
(12.) Vouge M, Pasquini U, Salvolini U. CT findings of atypical forms of phakomatosis. Neuroradiology. 1980;20:99-101.
(13.) Stavrou T, Dubovsky EC, Reaman GH, et al. Intracranial calcifications in childhood medulloblastoma: Relation to nevoid basal cell carcinoma syndrome. AJNR Am J Neuroradiol. 2000;21:790-794.
(14.) Gardeur D, Palmieri A, Mashaly R. Cranial computed tomography in the phakomatoses. Neuroradiology. 1983;25:293-304.
(15.) Savy LE, Moseley IF. Intracranial arterial calcification and ectasia in visual failure. Br J Radiol. 1996;69:394-401.
(16.) Yu YL, Chiu EK, Woo E, et al. Dystrophic intracranial calcification: CT evidence of 'cerebral steal' from arteriovenous malformation. Neuroradi ology. 1987;29:519-522.
(17.) Yamamoto M, Jimbo M, Ide M, et al. Gamma knife radiosurgery in cerebral arteriovenous malformations: Postobliteration nidus changes observed on neurodiagnostic imaging. Stereotact Funct Neurosurg. 1995;64 (Suppl 1):126-133.
(18.) Tomlinson FH, Rufenacht DA, Sundt TM Jr, et al. Arteriovenous fistulas of the brain and the spinal cord. J Neurosurg. 1993;79:16-27.
(19.) Shaida AM, McFerran DJ, da Cruz M, et al. Cavernous haemangioma of the internal auditory canal. JLaryngol Otol. 2000;114:453-455.
(20.) Nakase H, Morimoto T, Tsunoda S, et al. Cortical and subcortical cavernous angioma: A comparison of patients with and without hemorrhage as the initial symptom. Neurol MedChir. (Tokyo) 1992;32:196-200.
(21.) Fontaine S, de la Sayette V, Gianfelice D, et al. CT, MRI, and angiography of venous angiomas: A comparative study. Can Assoc Radiol J. 1987;38: 259-263.
(22.) Ramina R, Ingunza W, Vonofakos D. Cystic cerebral cavernous angioma with dense calcification. Case report. J Neurosurg. 1980;52:259-262.
(23.) Runnels JB, Gifford DB, Forsberg PL, Hanberry JW. Dense calcification in a large cavernous angioma. Case report. J Neurosurg. 1969;30:293-298.
(24.) Yasui T, Komiyama M, Nishikawa M, et al. Fusiform vertebral artery aneurysms as a cause of dissecting aneurysms. Report of two autopsy cases and a review of the literature. J Neurosurg. 1999;91: 139-144.
(25.) Terada S, Ishizu H, Tanabe Y, et al. Plaque-like structures and arteriosclerotic changes in "diffuse neurofibrillary tangles with calcification." Acta Neuropathol. 2001;102:597-603.
(26.) Collins AT, Cromwell LD. Computed tomography in the evaluation of congenital cerebral toxoplasmosis. J Comput Assist Tomogr. 1980;4:326-329.
(27.) Patel DV, Holfels EM, Vogel NP, et al. Resolution of intracranial calcifications in infants with treated congenital toxoplasmosis. Radiology. 1996;199: 433-440.
(28.) Kaufman WM, Sivit CJ, Fitz CR, et al. CT and MR evaluation of intracranial involvement in pediatric HIV infection: A clinical-imaging correlation. AJNR Am J Neuroradiol. 1992;13:949-957.
(29.) Benator RM, Magill HL, Gerald B, et al. Herpes simplex encephalitis: CT findings in the neonate and young infant. AJNR Am J Neuroradiol. 1985;6: 539-543.
(30.) Dublin AB, Merten DF. Computed tomography in the evaluation of herpes simplex encephalitis. Radiology. 1977;125:133-134.
(31.) Wasay M, Kheleani BA, Moolani MK, et al. Brain CT and MRI findings in 100 consecutive patients with intracranial tuberculoma. J Neuroimaging. 2003;13:240-247.
(32.) DeCarli C, Civitello LA, Brouwers P, et al. The prevalence of computed tomographic abnormalities of the cerebrum in 100 consecutive children symptomatic with the human immune deficiency virus. Ann Neurol. 1993;34:198-205.
(33.) Caldemeyer KS, Mathews VP, Edwards-Brown MK, Smith RR. Central nervous system cryptococcosis: Parenchymal calcification and large gelatinous pseudocysts. AJNR Am J Neuroradiol. 1997; 18:107-109.
(34.) Tien RD, Chu PK, Hesselink JR, et al. Intracranial cryptococcosis in immunocompromised patients: CT and MR findings in 29 cases. AJNR Am J Neuroradiol. 1991;12:283-289.
(35.) Raymond AA, Zariah AA, Samad SA, et al. Brain calcification in patients with cerebral lupus. Lupus. 1996;5:123-128.
(36.) Ricci P. Imaging of adult brain tumors. Neuroimaging Clin N Am. 1999;9:651-669.
(37.) Okuchi K, Hiramatsu K, Morimoto T, et al. Astrocytoma with widespread calcification along axonal fibers. Neuroradiology. 1992;34:328-330.
(38.) Luh YG, Bird CR. Imaging of the brain tumors in the pediatric population. Neuroimaging Clin NAm. 1999;9:691-716.
(39.) Smirniotopoulos JG. The new WHO classification of brain tumors. Neuroimaging Clin N Am. 1999;9:595-613.
(40.) Vonofakos D, Marcu H, Hacker H. Oligodendrogliomas: CT patterns with emphasis on features indicating malignancy. J Comput Assist Tomogr. 1979;3:783-788.
(41.) Reiche W, Grunwald I, Hermann K, et al. Oligodendrogliomas. Acta Radiol. 2002;43:474-482.
(42.) Brunette WC, Nesbit GM, Hall F. Pathologic correlation in oligodendroglioma. Int J Neuroradiol. 1997;3:503.
(43.) Meyers SP, Kemp SS, Tarr RW. MR imaging features of medulloblastomas. AJR Am J Roentgenol. 1992;158:859-865.
(44.) Peretti-Viton P, Perez-Castillo AM, Raybaud C, et al. Magnetic resonance imaging in gangliogliomas and gangliocytomas of the nervous system. J Neuroradiol. 1991;18:189-199.
(45.) Zentner J, Wolf HK, Ostertun B, et al. Gangliogliomas: Clinical, radiological, and histopathological findings in 51 patients. J Neurol Neurosurg Psychiatry. 1994;57:1497-1502.
(46.) Castillo M, Davis PC, Takei Y, Hoffman JC. Intracranial ganglioglioma: MR, CT, and clinical findings in 18 patients. AJNR Am J Neuroradiol. 1990;11:109-114.
(47.) Ostertun B, Wolf HK, Campos MG, et al. Dysembryoplastic neuroepithelial tumors: MR and CT evaluation. AJNR Am J Neuroradiol. 1996;17:419-430.
(48.) Tomita T, Larsen MB. Calcified metastases to the brain in a child: Case report. Neurosurgery. 1983;13:435-437.
(49.) Sastre-Garriga J, Tintore M, Montaner J, et al. Calcified cerebral metastases. Study of two cases and review of the literature. Neurologia. 2000;15: 136-139.
(50.) Kizana E, Lee R, Young N, et al. A review of the radiological features of intracranial meningiomas. Australas Radiol. 1996;40:454-462.
(51.) Hope JK, Armstrong DA, Babyn PS, et al. Primary meningeal tumors in children: Correlation of clinical and CT findings with histologic type and prognosis. AJNR Am J Neuroradiol. 1992;13:1353-1364.
(52.) Chiechi MV, Smirniotopoulos JG, Mena H. Pineal parenchymal tumors: CT and MR features. J Comput Assist Tomogr. 1995;19:509-517.
(53.) Zee CS, Segall H, Apuzzo M, et al. MR imaging of pineal region neoplasms. J Comput Assist Tomogr. 1991;15:56-63.
(54.) Tsuda M, Takahashi S, Higano S, et al. CT and MR imaging of craniopharyngioma. Eur Radiol. 1997;7:464-469.
(55.) Gao PY, Osborn AG, Smirniotopoulos JG, Harris CP. Radiologic-pathologic correlation. Epidermoid tumor of the cerebellopontine angle. AJNR Am J Neuroradiol. 1992;13:863-872.
(56.) Fujimaki T, Matsutani M, Funada N, et al. CT and MRI features of intracranial germ cell tumors. J Neurooncol. 1994;19:217-226.
(57.) Kinoshita Y, Yasukouchi H, Tsuru E, Yamaguchi R. Case report of Rosai-Dorfman disease mimicking pachymeningitis. No Shinkei Geka. 2004;32: 1051-1056.
(58.) Tamaki T, Takumi I, Kitamura T, et al. Pituitary stone--case report. Neurol Med Chir. (Tokyo) 2000; 40:383-386.
(59.) Dean B, Drayer BP, Beresini DC, Bird CR. MR imaging of pericallosal lipoma. AJNR Am J Neuroradiol. 1988;9:929-931.
(60.) Truwit CL, Barkovich AJ. Pathogenesis of intracranial lipoma: An MR study in 42 patients. AJR Am J Roentgenol. 1990;155:855-864.
(61.) Ganti SR, Antunes JL, Louis KM, Hilal SK. Computed tomography in the diagnosis of colloid cysts of the third ventricle. Radiology. 1981;138:385-391.
(62.) Koeller KK, Sandberg GD; Armed Forces Institute of Pathology. From the archives of the AFIP. Cerebral intraventricular neoplasms: Radiologicpathologic correlation. Radiographics. 2002;22: 1473-1505.
(63.) Van Tassel P, Lee YY, Bruner JM. Supratentorial ependymomas: Computed tomographic and pathologic correlations. J Comput Tomogr. 1986;10: 157-165.
(64.) Swartz JD, Zimmerman RA, Bilaniuk LT. Computed tomography of intracranial ependymomas. Radiology. 1982;143:97-101.
(65.) Chiechi MV, Smirniotopoulos JG, Jones RV. Intracranial subependymomas: CT and MR imaging features in 24 cases. AJR Am J Roentgenol. 1995;165:1245-1250.
(66.) Furie DM, Provenzale JM. Supratentorial ependymomas and subependymomas: CT and MR appearance. J Comput Assist Tomogr. 1995;19: 518-526.
(67.) Goergen SK, Gonzales MF, McLean CA. Interventricular neurocytoma: Radiologic features and review of the literature. Radiology. 1992;182: 787-792.
(68.) Yasargil MG, von Ammon K, von Deimling, et al. Central neurocytoma: Histopathological variants and therapeutic approaches. J Neurosurg. 1992;76: 32-37.
(69.) Swartz JD, Faerber EN, Singh N, Polinsky MS. CT demonstration of cerebral subcortical calcifications. J Comput Assist Tomogr. 1983;7:476-478.
(70.) Karimi M, Habibzadeh F, De Sanctis V. Hypoparathyroidism with extensive intracerebral calcification in patients with beta-thalassemia major. J PediatrEndocrinolMetab. 2003;16:883-886.
(71.) Fujita T. Mechanism of intracerebral calcification in hypoparathyroidism. Clin Calcium. 2004;14: 55-57.
(72.) Ogi S, Fukumitsu N, Tsuchida D, et al. Imaging of bilateral striopallidodentate calcinosis. Clin Nucl Med. 2002;27:721-724.
(73.) Sue CM, Crimmins DS, Soo YS, et al. Neuroradiological features of six kindreds with MELAS tRNA(Leu) A2343G point mutation: Implications for pathogenesis. J Neurol Neurosurg Psychiatry. 1998;65:233-240.
Erini Makariou, MD, and Athos D. Patsalides, MD
Dr. Makariou is an Associate Professor of Radiology, Department of Radiology, Georgetown University Hospital, Washington, DC. and Dr. Patsalides is an Assistant Professor of Radiology in Neurological Surgery, Weill Cornell Medical College, New York, NY.
Table 1. Intracranial calcifications Physiologic Posttraumatic and dystrophic Subdural/epidural hematoma Radiation/chemotherapy Ischemia/infarct Congenital disorders (phakomatoses) Neurofibromatosis I and II Tuberous sclerosis Basal cell nevus syndrome Sturge-Weber syndrome Vascular disorders Vascular malformations: AVM/AVF, cavernous angioma, venous angioma, and capillary telengiectasia Aneurysm Intracranial atherosclerosis Ischemia/infarct Vein of Gallen malformation Infections Congenital: CMV, toxoplasmosis, HIV, herpes Acquired: Cysticercosis, tuberculosis, HIV, cryptococcosis Inflammatory disorders Sarcoidosis Systemic lupus erythematosus Tumors Intra-axial: Astrocytomas, oligodendroglioma, medulloblastoma, gangli oglioma, DNET, metastases Extra-axial: Meningioma, pineal tumors, pituitary tumors, craniopharyngioma, epidermoid/dermoid, teratoma, colloid cyst, lipoma, metastases Intraventricular: Ependymoma, choroid plexus tumors, central neurocytoma, metastases Metabolic Hyperparathyroidism Hypoparathyroidism Hypothyroidism Fahr disease MELAS syndrome Table 2. Basal ganglia calcifications Physiologic/normal senescent (most common) Metabolic Hypoparathyroidism (including pseudo- and pseudopseudo hypoparathyroidism) Hyperparathyroidism Hypothyroidism Lead toxicity Fahr disease Hallevorden Spatz disease Ischemic Carbon monoxide intoxication Birth anoxia Infectious AIDS TORCH encephalitis Toxoplasmosis Cysticercosis Congenital Trisomy 21 Tuberous sclerosis Neurofibromatosis Chemotherapy (methotrexate) Radiation therapy
|Gale Copyright:||Copyright 2009 Gale, Cengage Learning. All rights reserved.|