Health &health

1. Dr/ ABD ALLAH NAZEER. MD.
Radiological imaging of intra-cranial calcification.

2. Normal intracranial calcifications
1- Normal intracranial calcifications can be defined as all age-related
physiologic and neurodegenerative calcifications that are unaccompanied
by any evidence of disease and have no demonstrable pathological cause.
The most common sites include:
pineal gland
seen in 2/3 of the adult population and increases with age
calcification over 1cm in diameter or under nine years old may be
suggestive of a neoplasm
habenula
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
choroid plexus
a very common finding, usually in the atrial portions of the lateral
ventricles
calcification in the third or fourth ventricle or patients less than nine
years of age is uncommon

3. basal ganglia calcification
are usually incidental idiopathic findings that have an incidence
of ~1% (range 0.3-1.5%) and increases with age
usually, demonstrate a faint punctuate or a coarse
conglomerated symmetrical calcification pattern
see basal ganglia calcification for specific differential
falx, dura mater or tentorium cerebelli
occur in ~10% of the elderly population
dural and tentorial calcifications are usually seen in a laminar
pattern and can occur anywhere within the cranium
petroclinoid ligaments
common age-related degeneration sites and usually have
laminar or mildly nodular patterns
superior sagittal sinus
common age-related degeneration sites and usually have
laminar or mildly nodular patterns

4. 2. Post-traumatic. They are chronic sequels after ischemic or parenchymal
hemorrhage from infarcts, trauma or surgery. In post radiation or chemotherapy
calcification appear long time after treatment and are much more common in
young children.
3. Congenital disorders (phakomatoses) - are hereditary disorders with multiple
central nervous system and cutaneous abnormalities. Calcifications are commonly
reported in tuberous sclerosis and Sturge-Weber syndrome, but can also appear in
basal-cell nevus syndrome and neurofibromatosis type I and II.
Tuberous sclerosis is a multisystemic autosomal-dominant disorder with typical
manifestation of the triad: seizures, mental retardation, and facial angiofibroma.
Neurofibromatosis type 1 is a multisystem neurocutaneous disorder associated
with increased incidence of different tumors, such as optic nerve glioma and
plexiform neurofibroma.
Neurofibromatosis type II (MISME - multiple intracranial schwannomas,
meningiomas and ependymomas). The most common calcifications seen in
neurofibromatosis type 2 are the ones associated with disease-related tumors,
such as meningiomas or ependymomas. Non tumoral calcifications are mainly
nodular calcifications of the cerebellum, symmetric / often asymmetric
calcifications of the choroid plexus and seldom cortical calcifications.
Sturge-Weber syndrome also known as encephalotrigeminal angiomatosis, is the
only phakomatoses that is not associated with intracranial neoplasms.

5. 4. Vascular disorders. Intracranial atherosclerosis. The presence of
calcifications in the arterial wall of large intracranial vessels should
be mentioned in radiologist report because of their association with
atherosclerosis. The carotid siphon (~60%) is the most commonly
affected vessel, calcifications in the vertebral artery (~20%) and
middle cerebral arteries (~5%) are less common.[2,3] Other causes
of vascular intracranial calcifications include: Aneurysm: although
patent aneurysms may contain mural calcification, partially or
entirely thrombosed aneurysms commonly have calcification.
Arteriovenous malformation: are arterio-venous shunting with no
capillary bed interfering. They may contain dystrophic calcification
along the tortuous vessels and within the adjacent parenchyma
with prevalence of 25 - 30%.[11] Cavernous malformation: are
abnormal clusters of low-pressure blood vessels embedded in
normal brain tissue. Occasionally have been described intracranial
calcification in developmental venous anomaly (DVA), and capillary
telangiectasia

6. 5. Infections. Patient with congenital infection present intracranial
calcification with no specific appearance, often similar to any chronic
brain injury (dystrophic calcifications). Calcifications in basal ganglia
and the cortex are common features of all diseases that compose the
TORCH syndrome (toxoplasmosis, other, rubella, cytomegalovirus,
herpes simplex virus). Calcifications in patients infected with
toxoplasmosis may resolve after treatment. The intracranial
calcifications patterns in acquired infections, although not specific are
extremely useful in making the correct diagnosis and evaluating
disease progression. Cysticercosis, tuberculosis, HIV and cryptococcus
are the most common disease typically associated with calcifications.
6. Inflammatory disorders. Systemic lupus erythematosus. In systemic
lupus erythematosus cerebral calcifications has been seen in the basal
ganglia, centrum semiovale, cerebellum and thalamus.
Neurosarcoidosis. The neurosarcoidosis lesion appearance is
nonspecific; granulomatous masses are seen as hyperdense nodules or
calcification and involves the parenchyma, nerve, the leptomeninges,
and dura matter.

7. 7. Tumors. Intra-axial: oligodendroglioma, astrocytomas, medulloblastoma,
ganglioglioma, 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. The most common intracranial neoplasms associated
with calcifications are oligodendroglioma (70-90%), craniopharyngioma (50-80%),
germ cell neoplasms, ganglioglioma (35-50%), meningioma (20-25%), choroid
plexus papilloma (25%), medulloblastoma (20%), low grade astrocytoma (20%),
and pilocytic astrocytoma (10%). Calcifications are rarely described in
schwannomas, and dermoid and epidermoid tumor. Craniopharyngioma is a
benign tumor derived from Rathke,s pouch epithelium. Calcification is described
the hallmark of a craniopharyngioma and occurs in about 90% of tumors.
8. Metabolic/ endocrine pathologies.
Hyperparathyroidism/Hypoparathyroidism/Hypothyroidism/MELAS syndrome
Endocrine disorders involving calcium homeostasis are frequent associated with
intracranial calcification. Most common locations are the basal ganglia, but also
subcortical white matter, thalami and cerebellum. Fahr disease, a familial
cerebrovascular ferrocalcinosis, is a rare condition starting in childhood presenting
with progressive mental deterioration. It is characterised by extensive deposits of
iron and calcium in the globus pallidus, dentate nuclei and subcortical white
matter.

8. NECT (a) Calcified bilateral petroclinoid ligaments. (b) Small calcification along the tentorium.
(c) Bilateral choroid plexus (arrowheads), pineal and habenular (arrow) calcification.

9. Different pattern of pineal gland calcification: (a) nodular, (b) curvilinear, (c) punctate.

10. NECT Linear calcified falx cerebri.

11. Axial NECT in two patients. Different type of bilateral globus pallidus
calcifications (a) coarse conglomerated and (b) punctate.

12. Non-contrast CT of the head shows dense bilateral basal ganglia calcification (black arrows).

14. Right caudate head dense calcification in a 55 years old male.

15. Post surgery right frontal cortical(red arrows) and dural (white arrow) calcification in a patient with LMNH.

16. NECT in a patient with hydrocephaly (star). Left posttraumatic
dural calcification (after epidural hematoma)(arrow).

17. Right chronic (hypodense) subdural hematoma (stars).
NECT - small linear dural calcification (arrows)

18. Multiple calcified subependymal hamartomas along the lateral ventricles and foramen
of Monro in two different patient with tuberous sclerosis; (a ,c) infratentorial small
calcification (b, d) supratentorial partial calcified subcortical tuber (white arrow).

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

20. Multiple calcified subependymal hamartomas along the lateral
ventricles and foramen of Monro.

21. Neurofibromatosis Type I; (a)NECT - Multiple small intracerebral calcification,
widened optic nerve foramina (large white arrow), (b) MRI with Gd shows
multiple intracerebral tumoral lesions (red arrows) little enhancement(green
arrows) and enlarged optic nerves and optic chiasm (small white arrow).

22. Plain lateral skull radiograph demonstrates the typical gyriform
pattern of cortical calcification (arrows) in the occipital region.

23. (a) X-ray lateral view of skull showing 'tram-track' calcification. (b) Computed tomography (CT) scan
of brain showing atrophy and extensive gyral pattern of calcification of left cerebral hemisphere

24. M 55 y, presenting facial angioma and epilepsy. NECT reveal typical left frontoparietal gyral calcification
in Sturge-Weber Syndrome (red arrows); left fontal lobe atrophy associated (white arrow).

26. Sturge-Weber, Gyriform cortical calcifications with ipsilateral atrophy and enlarged choroid plexus.

27. Megadolico vertebro-basilar system and internal carotid artery
with multiple small atherosclerotic calcified plaques.

28. Calcified plaques in the wall of vertebrobasilar system and bilateral
internal carotid (red arrows), middle cerebral artery (white arrow)

29. Plain X rays of skull. (a) and (b) Curvilinear midline
calcification in the wall of aneurysm of vein of Galen.

30. Giant left middle cerebral artery thrombosed aneurysm(red arrows). (a) NCET, Rim like wall calcification
and granulosus calcification; moderate edema developed in temporo-insular left region, (b)MRI and (c)
CECT confirming partial thrombosed aneurysmal; enhanced residual lumen (green arrow).

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

32. Angio-CT: MIP and source image - complex vascular malformation: aneurysm of the pericallosal
artery and partially thrombosed saccular venous dilatation with peripheral calcifications (arrows).

33. Developmental venous anomaly. Right cerebellar hemisphere heterogeneous lesion with small
hypodense central area, multiple serpentines vascular calcification (red arrows), vascular tracks
with "medusa head" sketch located peripheral with intense enhancement (white arrows).

34. Cavernous malformation. (a) NECT Small hyperintense lesion, with punctate
calcification in left periventricular white matter, near occipital lateral ventricle horn.
(b )MRI. "Popcorn" appearance with hypointense hemosiderin rim on T2-wi (green
arrow); T1-wi with Gd - shows small venous malformation associated (white arrow).

35. Massive calcifications in right frontal lobe colon cancer metastasis.

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

37. Obstructive craniopharyngioma. Axial NECT (a)- Heterogenous suprasellar masse with peripheral
calcification (red arrows) and hypodense area; hydrocephaly associated(star); (b) CECT - Little
enhancement (small white arrows) and mild displacement of Circle of Willis (large white arrow).

38. Large left parasellar meningioma. (a) NECT heterogenous mass with diffuse
calcification, (b) MRI with Gd- homogenous enhancement (white arrow).

39. NECT - large left meningioma in two different patient with (a)
circular calcification pattern and (b) radial calcification pattern.

40. Meningioma. (a) NECT Large left meningioma with radial
pattern calcification, (b) CECT - homogenous enhancement.

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

42. AP X-ray of the skull (2A) and lateral (2B) view show a ghost-like appearance (‘alien look’)
with cranial hyperostosis (black arrowheads). Focal bilateral symmetrical intracranial
calcification is seen (black arrows). Thinned out and focally absent enamel with missing teeth
and cavities are seen (thin white arrows) with broadened mandible (thick white arrow).

43. Pericallosal and interhemispheric lipoma with calcification.

44. Rare idiopathic disorders such as Fahrs disease.

45. Congenital infections with intra-cranial calcification.

46. Occipital Calcification with neonatal thyrotoxicosis.

47. Nonenhanced (left) and enhanced (right) CT scans of the brain in a patient with
neurocysticercosis show multiple ring-enhancing lesions with perifocal edema.

48. Nonenhanced (left) and enhanced (right) CT images of the brain in a patient with
neurocysticercosis show an enhancing disk lesion with perifocal edema suggestive
of the granulomatous form of disease (arrow). Multiple ring lesions are also
apparent; these are suggestive of the colloid stage of neurocysticercosis.

49. CT images of the brain in a patient with neurocysticercosis show numerous parenchymal lesions.

50. Cockayne syndrome with extensive intracranial calcification

51. (A) Magnetic resonance axial section T2* GRE sequence with extensive brain calcification.
(B) Computed tomography scan axial section with basal ganglia calcification.

52. An 8-year-old male with a
long complicated medical
history was found to have
hard-to-miss calcifications
on the plain skull x-ray (a,
d). The NCECT (b, e) and 3D
reconstructions (c, f) show
a large amorphous
calcification originating
from the basal ganglia,
extending into the right
lateral ventricle of the
patient diagnosed with
tuberous sclerosis.
Subependymal nodules
associated with tuberous
sclerosis can calcify with
age, typically presenting
with globular or
sometimes ring-like
calcification.

53. A 17-year-old female with
seizures presented with a
large calcified mass
apparently arising from the
left temporal lobe. The
calcification pattern (mostly
peripheral) and morphology
(“popcorn appearance”)
strongly suggested a vascular
lesion such as a cavernous
malformation (cavernous
angioma) or, less likely, a
calcified haemangioma. Upon
excision, the mass was later
found to be a choroid plexus
papilloma, shown in the axial
NCECT in soft tissue (a) and
bone windows (b) as well as
the coronal NCECT
reconstruction in soft
tissue (c) and bone
windows (d)

54. A 60-year-old male
known HIV patient
presented with seizures.
The solid calcifications
on NCECT at the right
frontal (a) left basal
ganglia(b) and right
parietal
areas (c) represent
sequelae following
treatment for
documented
toxoplasmosis. 3D
reconstruction (d). In
congenital
toxoplasmosis,
calcifications have been
shown to decrease in
size or even completely
resolve with treatment

55. An adult case of leukoencephalopathy with intracranial calcification and cyst.

58. Pachygyria, and cerebellar hypoplasia, B: generalized intracranial
calcification, C: intracranial calcification and cerebellar hypoplasia.

59. 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.

60. Thank You.