Intracranial calcifications

Erini Makariou, MD, and Athos D. Patsalides, MD

Summary:  In this article, the authors demonstrate a broad spectrum of common and uncommon central nervous system disorders associated with calcifications. In order to provide a systematic review and an approach to a more accurate diagnosis, they present the intracranial calcifications according to the underlying etiology, and the neoplastic processes are subdivided according to location.

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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.

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).

Physiologic calcifications

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 years1 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 thedura (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

Dystrophic calcifications

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 rapidlycalcified epidural hema- tomas.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 calcificationshave been observed:

  • mineralizing microangiopathy, which affects small arteries and arterioles, resulting in basal ganglia and subcortical white-matter calcifications;
  • 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 hem-orrhage from trauma, and prior surgery are alsoassociated with dystrophic calcifications.

Congenital disorders/phakomatoses

The phakomatoses are a group of hereditary disorders that affect structures of ectodermal origin. Classically, calcifications are described intuberous 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 thecaudate 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 subepen-dymal and cortical hamartomas are rare during the first year of life and the rate increases along with the patient’s age.

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 postcontrast images and are located at ornear 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 cerebellum11 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.

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% ofpatients these calcifications are bilateral.14

Vascular calcifications

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, suchas vascular malformations and aneurysms.

Atherosclerosis is associated with mural calcifications of the major intra-cranial 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 cana lso 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 calcifications19 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 fusiform24 compared with saccular aneurysms. Amyloid angiopathy results in gyriform calcification and sclerotic changes in the medullary arteries.25

Congenital infections

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 peri-ventricular 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 cortical29 or extensive gyral calcifications.30

Acquired infections

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 parenchyma33 and the leptomeninges.34

Inflammatory lesions

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 (Figure17) has been associated with cerebral calcifications in the basal ganglia, thalamus, cerebellum and centrum semiovale.35

Tumors

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.

Intra-axial tumors

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.

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 gangliocytomas44 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

Extra-axial tumors

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.

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 cases55 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

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 tumors

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 extra-axial meningiomas.

Endocrine/metabolic/idiopathic

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 pseudo rather than idiopathic hypoparathyroidism.71 Hypothyroidism is also associated with basal ganglia and cerebellar calcifications.

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

Conclusion

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.

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Tables & Figures

  • Figure 1. Physiologic calcifications in a 51-year-old man with headache. Axial nonenhanced computed tomography (CT) image reveals physiologic calcifications of the basal ganglia bilaterally.
    Figure 1.
  • Figure 2. Physiologic calcifications in a 55-year-old woman with headache. Axial nonenhanced CT image reveals physiologic calcifications of the pineal gland and the choroid plexuses bilaterally.
    Figure 2.
  • Figure 3. Calcified falx in a 46-year-old woman with subarachnoid hemorrhage. Axial nonenhanced CT image shows dense calcifications of the anterior falx. Subarachnoid hemorrhage is seen in the sulci of the right parietal lobe.
    Figure 3.
  • Figure 4. Physiologic calcifications of the dentate nuclei in a 86-year-old woman. Axial nonenhanced CT image shows prominent symmetric calcifications in the dentate nuclei bilaterally.
    Figure 4.
  • Figure 5A. A 50-year-old man with chronic right subdural hematoma. Axial nonenhanced CT image (A) shows a chronic, right, subdural hygroma with calcifications along the inner surface. Axial CT image of the skull in bone windows (B) shows calcifications.
    Figure 5A.
  • Figure 5B.
    Figure 5B.
  • Figure 6A. A 21-year-old patient with tuberous sclerosis presents with seizures and mental retardation. Axial noncontrast CT image reveals calcified subependymal hamartomas along the lateral ventricles and the region of the foramina of Monro. The largest lesion adjacent to the left foramen of Monro is a giant cell astrocytoma.
    Figure 6A.
  • Figure 6B.
    Figure 6B.
  • Figure 7.  A 21-year-old patient with basal cell nevus syndrome. Axial noncontrast CT image shows dense calcification along the falx.
    Figure 7.
  • Figure 8A. A 6-year-old boy with Sturge-Weber syndrome. Posterioanterior radiograph (A) of the skull shows tram-track calcifications of the right side of the head. Axial nonenhanced CT image (B) shows dense gyriform calcifications in the cortex of the right frontotemporal region with associated brain volume loss. There is compensatory dilatation of the right lateral ventricle.
    Figure 8A.
  • Figure 8B.
    Figure 8B.
  • Figure 9. Atherosclerosis of the intracranial arteries in a 70-year-old man.  Axial nonenhanced CT image (bone algorithm) shows wall calcifications of the supraclinoid internal carotid arteries.
    Figure 9.
  • Figure 10. Atherosclerosis of the left vertebrobasilar system in a 41-year-old man with lymphoma, status post kidney transplantation. Axial nonenhanced CT image reveals an elongated prominent left vertebrobasilar artery with wall calcifications.
    Figure 10.
  • Figure 11A. Cavernous angioma in the pons of a 30-year-old man with headaches. Axial nonenhanced CT image (A) reveals a round hyperdense lesion with punctate calcifications in the pons. There is no associated mass effect or surrounding edema. Hyperdense foci in CSF spaces are Pantopaque residue from a previous myelogram. T2-weigheted (T2W) magnetic resonance (MR) image (B) at the level of the pons shows a lesion with mixed signal intensity and a rim of low signal intensity due to hemosiderin deposition.
    Figure 11A.
  • Figure 11B.
    Figure 11B.
  • Figure 12A. Calcifications related to a venous angioma in a 50-year-old woman with headaches. Axial nonenhanced CT image (A) shows a wedge-shaped calcified area in the left frontal lobe. Coronal nonenhanced T1-weighted (T1W) MR image (B) reveals the classic appearance of a venous angioma in the left frontal lobe (arrow).
    Figure 12A.
  • Figure 12B.
    Figure 12B.
  • Figure 13A. A 75-year-old man with a giant thrombosed left ICA aneurysm. Lateral radiograph of the skull (A) shows a round lesion with rim calcifications in the suprasellar region. Coronal postcontrast CT image (B) shows a peripherally calcified round lesion in the suprasellar region without enhancement. The left middle and anterior cerebral arteries are not visualized. Lateral view of a left carotid angiogram (C) reveals no enhancement of the round calcified lesion.
    Figure 13A.
  • Figure 13B.
    Figure 13B.
  • Figure 13C.
    Figure 13C.
  • Figure 14. Congenital toxoplasmosis in a 6-year-old boy with seizures and mental retardation. Axial noncontrast CT image reveals dense calcifications in the basal ganglia and subcortical white matter bilaterally. There is brain volume loss with colpocephaly.
    Figure 14.
  • Figure 15A. A 5-year-old boy with congenital HIV infection with generalized atrophy. Axial nonenhanced CT image (A) shows calcifications in the subcortical white matter of the frontal lobes and the dentate nuclei. Axial nonenhanced CT image (B) shows additional calcifications in the basal ganglia bilaterally.
    Figure 15A.
  • Figure 15B.
    Figure 15B.
  • Figure 16A. Cysticercosis in a 32-year-old man with seizures and headaches. Axial nonenhanced CT image (A) shows several punctuate calcifications in the parenchyma and along the left frontal horn. Axial nonenhanced CT image (B) shows several punctuate calcifications in the parenchyma. Axial contrast-enhanced T1W MR image (C) shows enhancement of the left frontal horn lesion (arrow). Coronal contrast-enhanced T1W MR image (D) shows an enhancing lesion in the right temporal lobe (arrow).
    Figure 16A.
  • Figure 16B.
    Figure 16B.
  • Figure 16C.
    Figure 16C.
  • Figure 16D.
    Figure 16D.
  • Figure 17A. A 42-year-old woman with systemic lupus erythematosus. Axial nonenhanced CT image (A) shows calcifications in the basal ganglia bilaterally. Axial nonenhanced CT image (B) shows faint linear calcifications along the lenticulostriate vessels.
    Figure 17A.
  • Figure 17B.
    Figure 17B.
  • Figure 18.  A low-grade astrocytoma in a 75- year-old woman. Axial nonenhanced CT image shows a left posterior frontal/parietal mass with dense calcifications, surrounding edema and mass effect on adjacent parenchyma.
    Figure 18.
  • Figure 19.  Gliobastoma multiforme in a 44-year-old. Axial nonenhanced CT image shows a heterogenous lesion with peripheral irregular calcifications in the left basal ganglia region with a large zone of surrounding vasogenic edema. The lesion produces mass effect on the lateral ventricles and midline shift to the right.
    Figure 19.
  • Figure 20. A 35-year-old man with left frontal oligodendroglioma and history of seizures. Axial nonenhanced CT image shows a round lesion with peripheral calcifications and a small surrounding zone of edema.
    Figure 20.
  • Figure 21A. A 25-year-old man with ganglioglioma in the right temporal lobe. Axial nonenhanced CT image (A) shows a completely calcified lesion in the right temporal lobe without associated edema or mass effect. Axial nonenhanced CT image (B, bone algorithm) shows the densely calcified lesion in the right temporal lobe.
    Figure 21A.
  • Figure 21B.
    Figure 21B.
  • Figure 22A. Calcified brain metastases in a 65-year-old-man with prostate cancer. Axial nonenhanced CT image (A) shows a dense calcified lesion with surrounding vasogenic edema in the left frontal lobe. A calcified focus is seen in the right frontal lobe. Axial nonenhanced CT image (B) shows calcified lesions with a small zone of edema in both parietal lobes.
    Figure 22A.
  • Figure 22B.
    Figure 22B.
  • Figure 23A. A 58-year-old woman with a calcified occipital meningioma. Axial nonenhanced CT image (A) shows a calcified, broad-based, extra-axial lesion in the occipital regions. Axial nonenhanced CT image (B, bone algorithm) shows the calcified lesion in the occipital regions.
    Figure 23A.
  • Figure 23B.
    Figure 23B.
  • Figure 24. A 69-year-old woman with partially calcified meningioma. Axial nonenhanced CT image shows a broad-based, partially calcified, extra-axial lesion in the right cerebellopontine angle. There is associated hyper- ostosis of the petrous bone and mass effect on the pons and right cerebellum.
    Figure 24.
  • Figure 25A. Small suprasellar calcified meningioma in a 78-year-old woman. Axial nonenhanced CT image (A) shows a round, well-defined, calcified lesion in the suprasellar region. Axial nonenhanced CT image (B, bone algorithm) shows the calcification.The same lesion on MRI is isointense on T1W and hypointense on T2W images with a dural tail and minimal peripheral enhancement (not shown).
    Figure 25A.
  • Figure 25B.
    Figure 25B.
  • Figure 26A. Peripherally calcified craniopharyngioma in a 55-year-old woman complaining of headaches and vision disturbances. Axial nonenhanced CT image (A) shows a round, peripherally calcified lesion compromising the third ventricle, resulting in obstructive hydrocephalus. Coronal postcontrast T1W MR image (B) shows the suprasellar lesion with an enhancing rim.
    Figure 26A.
  • Figure 26B.
    Figure 26B.
  • Figure 27. Calcified central neurocytoma in a 35-year-old with headaches. Axial nonenhanced CT image shows a densely calcified, well-defined, irregularly shaped mass in the region of the septum pellucidum and left frontal horn. The left frontal horn is enlarged.
    Figure 27.
  • Figure 28. A 45-year-old woman with intraventricular meningioma. Axial nonenhanced CT image shows a well-defined, ovoid, densely calcified lesion in the region of the third ventricle extending into the frontal horns. There is mild dilatation of the lateral ventricles.
    Figure 28.
  • Figure 29A. Progressive brain calcifications in a 31-year-old HIV-positive patient with renal failure on dialysis. Axial nonenhanced CT image (A) shows punctuate calcifications in the globus pallidus bilaterally and along the posterior falx. Calcifications are also seen along the tentorium, bilaterally (B). Five months later, another CT study of the head (C) showed marked progression of these calcifications in the globus pallidus, along the posterior falx and the tentorium bilaterally (D).
    Figure 29A.
  • Figure 29B.
    Figure 29B.
  • Figure 29C.
    Figure 29C.
  • Figure 29D.
    Figure 29D.
  • Figure 30A. A 50-year-old man with hypoparathyroidism. Nonenhanced axial CT image (A) shows areas of calcifications in the subcortical white matter and the basal ganglia. Nonenhanced axial CT image (B) shows areas of calcifications in the subcortical white matter and the basal ganglia.
    Figure 30A.