Knowledge of physiologic calcifications in the brain parenchyma is essential to avoid misinterpretations.

1. Intracranial calcificitation on
CT
Dr K KABULO

3. 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.

4.  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

5. Age-related physiologic and
neurodegenerative calcifications
 Intracranial physiologic calcifications
are unaccompanied by any evidence
of disease and have no demonstrable
pathological cause

6.  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)

7. The typical location are:
 the epiphysis
 Pineal gland
 habenula
 choroid plexus,
 tentorium
 petroclinoid ligaments
 falx cerebri
 basal ganglia
 sagittal sinus.

8. Calcification of the pineal
gland
 55% of patients> 20 yrs age have a
calcified pineal gland visible on plain
skull x-ray
 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

10. 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

12. Choroid plexus calcification
 Very common finding, usually in the
atrial portions of the lateral ventricles
 it 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

14. 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.

16. Basal ganglia calcifications
 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

19. 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
 Dural and tentorial calcifications are
usually seen in a laminar pattern and
can occur anywhere within the

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

22. 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’s syndromes
(GS).

23. Tuberous sclerosis
 cortical/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.

25. 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;

27. 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.

29. Neurofibromatosis type II
 Intracranial 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.

31. 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.

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

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

37. Developmental venous
anomaly
 represented by dilated medullary white
matter veins
 with "medusa head" aspect.
CT features:
 occasional small punctate
calcification;
 enhancing stellate tubular vessels
converging in collector vein.

39.  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

41. Infection
 cysticercosis
 encephalitis, meningitis, cerebral
abscess (acute and healed)
 granuloma (torulosis and other fungi)
 hydatid cyst
 tuberculoma
 paragonimiasis
 rubella
 syphilitic gumma

42. Infections
Congenital
 Cytomegalovirus 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.

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

44.  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

46.  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

48.  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

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

51. Tumors
 Neoplastic calcifications usually suggest a
more benign process
 meningioma
 craniopharyngioma
 choroid plexus papilloma
 ependymoma
 glioma (especially oligodendroglioma, also
astrocytoma)
 ganglioglioma
 lipoma of corpus callosum
 pinealoma
 hamartoma of tuber cinerium

52. Tumors
 Metastasis.Intracranial calcification
may occur from lung, breast, colon
cancer and osteogenic sarcoma.

53.  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.

55.  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

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

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

59.  Meningiomas About 25-30% of
meningiomas are fully calcified on CT.
 The calcifications are either focal or
diffuse, psammomatous, rim or have
radial pattern.

61. 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.

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

63.  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.

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

65.  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.

67. Miscellaneous
 hematoma: ICH, EDH or SDH.
Calcifications usually only when
chronic
 idiopathic

68. Conclusion
 1.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.

69. MERCI

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