Normal Pressure Hydrocephalus Imaging Findings

NPH
First described in 1965 by Hakim and Adams.
A clinical entity consist of the triad of 1) gait disturbance, 2) dementia, and 3) incontinence with normal cerebrospinal fluid (CSF) pressures and radiographic findings of Ventriculomegaly out of proportion to atrophy.
NPH is a relatively rare cause of dementia, but identifying NPH is important because it is one of the few treatable entities.

NPH on CT
Ventriculomegaly that is out of proportion to cortical atrophy, so called ventriculo sulcal disproportion. This differentiates NPH from age related ex vacuo dilatation of lateral ventricles which is mild and in proportion with atrophy.

In NPH, ventriculomegaly is prominent in all three horns of the lateral ventricles, third ventricle with relative sparing of the fourth ventricle.
Frontal and occipital periventricular low attenuating areas which may represent transependymal CSF flow may be noted in NPH, but this sign is infrequent and often difficult to differentiate from age related small vessel disease.

NPH on MRI
Ventriculomegaly out of proportion with sulcal atrophy is the hallmark.
But the MRI in addition to CT provides certain associated or supporting findings to favour NPH.
As per Tsunoda and colleagues study, 3-dimensional MRI volume-acquisition techniques can be used to objectively assess ventriculosulcal disproportion. But this volumetric analysis via MRI does not seem to help predict patient response to CSF shunting.
As per Jack and coworkers study, the predictive value of 3 MRI findings used with respect to positive response to CSF shunting, these studies included 1) CSF flow void sign, 2) Peri ventricular T2 hyper intensity and 3) Corpus callosal thinning on sagittal sections.

CSF flow void sign : On T2-weighted images, moving CSF demonstrate low signal similar to the flow void effects of vascular flow voids, common in cerebral aqueduct and in fourth ventricle seen as a focal absent signal in the Csf pool on T2w images due to jet of turbulent CSF.

Peri ventricular T2 hyper intensity : MRI FLAIR may show transependymal seppage of CSF in the form of a periventricular high signal primarily at the tip of frontal horns and occipital horns of the lateral ventricles, can be adequately differentiated from small vessel disease compared to CT.

Copus Callosal thinning : needs sagittal sections for evaluation of corpus callosum.










Conclusion: 
NPH is clinically characterized by triad of ataxia, dementia and incontinence. 
+ Imaging finding which are supportive and include Ventriculomegaly out of proportion with cortical atrophy, Corpus callosal thinning, CSF flow voids, Periventricular ooze of Csf.
+ Respond to Csf drainage via lumbar puncture. 

Sturge Weber Syndrome CT Brain

Clinical details: A 14 y o male with mental retardation, seizures and a pink patch on left side fore head.

This non contrast CT brain shows:
Left hemiatrophy.
Dense left temporo parietal cortical gyriform calcification.
Poor development of ipsilateral hemicranium, thickening of bony calvarium.
Enlargement of ipsilateral choroid plexus.
Hyperpneumatisation of left frontal sinus.

Clinical and imaging findings are very typical of Sturge Weber syndrome.

Related posts:
Sturge-weber-syndrome Case 1
Sturge-weber-syndrome Case 3
Mimics-of-sturge-weber-syndrome

Vertebrobasilar dolichoectasia

Non contrast 3 D TOF Angiogram of brain

VBDE refers to an abnormal elongation, dilatation and tortuosity of the vertebral and basilar arteries.
An anomaly secondary to defective tunica intima and occasionally the tunica media causes weakening of vessel walls resulting in elongation and dilatation of the artery.

Most commonly affects Vertebral Basilar Artery and elderly females.

• Criteria for dolichoectasia of verbrobasilar system, the basilar arterial diameter should be more than 4.5 mm.

Usually asymptomatic.
May present with CN compressions, most commonly affects VII and V CN.
Brain stem compression. Mid brain compression and obstructive hydrocephalus secondary to compression of aqueduct is also reported.

Fenestrated ACA

Non contrast 3 D TOF MR Angiogram of Brain

Fenestration is a window or a ring produced by a segment of an artery.

Duplication and fenestration of artery both are considered as rare developmental anomalies but are used incorrectly and interchangeably. 

Duplication should be strictly applied to the artery that has 2 origins and a variable course with or without reunion in the same anatomical area.

In contrast, fenestration represents a vessel with a single origin, anywhere along its course the main trunk divides and reunites again forming a window or a ring. 

Plexiform Neurofibroma Spine

A 31 yo male with progressive lower limb weakness.

MRI Lumbar spine show a neoplastic soft tissue completely occupying lumbo sacral spinal canal ,
Enhancement on post contrast T1,
Punctate low signal intensities on T2 and post contrast T1,
Expansion of spinal canal with marked posterior vertebral scalloping.
Extending out of neural foramen on either side.

Imagingwise diagnosis : Plexiform neurofibroma.

Grading small vessel disease

Fazeka's classification is used for grading of changes of small vessel disease.
MR is more sensitive and specific compared to CT, Axial FLAIR is enough.

Fazekas I : Mild, few small punctate lesions in the deep white matter.
Fazekas II : Moderate; larger WMLs that are beginning to become confluent.
Fazekas III : Severe; confluent T2 hyper intensity.

Grade i or Mild:

Grade ii or Moderate:

Grade iii or Severe:

Fazekas I is considered normal in aging after 40.

Fazekas II is considered abnormal in patients < 75 Years.

Fazekas III is abnormal in any age group and indicate poor control over diabetes and hypertension.

Cytotoxic vs Vasogenic odema

Cerebral odema is an excess accumulation of water in the intracellular and/or extracellular spaces of the brain.
There are four types of cerebral edema, but the cytotoxic and vasogenic odema are the two of most clinical importance and it is equally important to differentiated between the two.
Vasogenic odema: occurs due to the failure of tight junctions and astrocyte processes which normally maintain an adequate blood-brain barrier. Result in normally excluded intravascular proteins and fluid to penetrate into cerebral parenchymal extracellular space. Once these plasma constituents cross the BBB, the edema spreads fast and widespread. As water enters white matter it moves extracellularly along fiber tracts. Imagingwise this odema is seen as hypodensity confined to white matter, involve sub cortical white matter , spares cortical grey matter, and pronounces the grey white matter interphase.
This type of edema is seen in response to hemorrhagic contusion in cases of trauma, bleed, venous infarcts, late stages of cerebral ischemia where an associated hemorrhagic transformation occurs, tumors, focal inflammation, acute hypertensive encephalopathy.
Image gallery:

Mechanisms contributing to BBB dysfunction are 1. physical disruption by arterial hypertension result from direct transmission of pressure to cerebral capillary with transudation of fluid into the ECF (extracellular fluid) from the capillaries 2. Trauma with bleed, 3. tumor-facilitated release of vasoactive and endothelial destructive compounds like arachidonic acid, excitatory neurotransmitters, eicosanoids, bradykinin, histamine, free radicals; vascular endothelial growth factors (VEGFs) which weakens the junctions of the blood-brain barrier. Dexamethasonecan, a steroid is of benefit in reducing VEGF secretion.

Cytotoxic odema: In this type of edema the BBB remains intact. This edema is due to failure of ATP-dependent ion transport (sodium and calcium pumps). As a result there is cellular retention of sodium and water. Astrocytes get involved which occur in gray as well as white matter so Imaging wise cytotoxic odema seen as hypodensity involving cortical grey matter as well as white matter result in loss of normal grey white matter interphase. Cytotoxic edema is seen with various intoxications and early ischemia.
Image gallery:

Osmotic Odema: Normally CSF and brain’s extracellular fluid  osmolality is slightly lower than that of plasma. When plasma is diluted by excessive water, the brain osmolality will exceed the serum osmolality creating an abnormal pressure gradient result in water to flow into the brain causing edema. Causes include excessive water intake or  hyponatremia, syndrome of inappropriate antidiuretic hormone secretion (SIADH), hemodialysis, or rapid reduction of blood glucose in hyperosmolar hyperglycemic, hyperosmolar non-ketotic acidosis.

Interstitial Odema: Occurs in obstructive hydrocephalus, due to rupture of the CSF-brain barrier resulting in trans-ependymal flow of CSF, CSF penetrate the brain and spread to the extracellular spaces and the white matter. This is differentiated from vasogenic edema in that interstitial cerebral edema CSF contains almost no protein.
Image gallery:

Cytotoxic vs Vasogenic odema – imagingwise differentiation
Cytoxic odema seen in ischemia infarct, seen as an abnormal area of uniform low attenuation or abnormal signal intensity, area of involvement corresponds to particular vascular territory, involves cortical grey as well white matter, loss of normal grey white matter interphase.
Vasogenic oedema seen in around bleed, infective or inflammatory lesion like granuloma abscess, tumour, acute hypertensive encephalopathy. Seen as an abnormal area of low attenuation or abnormal signal intensity confined to white matter around the lesion, with finger like projections extending in sub cortical white matter. Spares overlying adjacent cortical grey matter.  Grey white matter interphase is pronounced instead of loss.

Hyperdense sinus on CT Brain

A 25 yo female C/o headache.

Hematocrit 77.6%

Hb 26.7 gm%. 

Non contrast CT shows abnormal hyperdensity in the region of superior sagittal sinus; ' Cord sign' or ' Dense triangle' sign. No other parenchymal abnormality. 

MRI Brain shows abnormal high signal in the region of superior sagittal sinus with loss of normal flow voids implies to thrombosis as corresponding sinus not visualized on non contrast 2 D TOF MR Venogram. 

In this case based on hematocrit and non contrast CT findings the other closest differential is polycythemia. 
Features of polycythemia on NCCT head includes increase in attenuation of venous sinuses may not be as hyperdense as in this case but is primarily a reflection of hemoconcentration and attenuation of the hemoglobin protein. 
Hyperdensity in the region of dural venous sinuses is typically seen in cerebral venous sinus thrombosis. Cerebral venous thrombosis is a known complication of polycythemia and hypercoagulable states and hence both may coexist. so polycythemia may mimic cerebral venous thrombosis on CT and polycythemia may cause cerebral venous thrombosis.
MR venography is required to differentiate between the two and rule out CVT. 

Reference : J Pediatr Neurosci. 2010 Jan-Jun; 5(1): 27–29. doi:  10.4103/1817-1745.66679; Healy JF, Nichols C. Polycythemia Mimicking Venous Sinus Thrombosis. AJNR Am J Neuroradiol.2002;23:1402–3. [PubMed]

CNS Tuberculosis

Involvement of CNS seen in approximately 5% of total patients of tuberculosis.
With greater prevalence immunocompromised patients, CNS involvement is seen in up to 15% of cases of acquired immunodeficiency syndrome – related tuberculosis.
CNS involvement usually results from hematogenous spread.
CNS tuberculosis various common forms include tuberculous meningitis, tuberculoma, Calcified tubercular granuloma, Abscesses, and in spine osseous involvement is more common than non osseous spinal cord and spinal meningeal involvement.

Classification of Brain and Spine tuberculosis: 
In brain

Tubercular Meningitis and its complications
Basal exudates.
Diffuse or focal lepto meningeal enhancement.
Patchy meningitis.
Hydrocephalus.
Vasculitis causing infarction
Cranial Neuropathies
Parenchymal Tuberculosis 
Tuberculomas.
Tubercular abscesses.
Miliary Tuberculomas.
Focal Cerebritis.
Tubercular Encephalopathy.
Tuberculoma en plaque.
Tubercular Hypophysitis.
Tuberculosis of Calvarium and skull base.
Orbital Tuberculosis
Otitis Media and temporal bone tuberculosis
In spine and spinal cord

Discitis.
Spondylodiscitis
Vertebral osteomyelitis.

Non osseous spinal tuberculomas.
Arachnoiditis.
Myelitis.


Tuberculous Meningitis
The most common manifestation of CNS tuberculosis across all age groups.
Early diagnosis is important to reduce morbidity and mortality.
Usually due to hematogenous spread but can also be secondary to rupture of a parenchymal focus or direct extension from cerebrospinal fluid.
Imaging finding include exudates most pronounced in the basal cisterns seen as hyper density on CT and hyperintensity on MRI Flair. Abnormal enhancement of exudates particularly in basal cisterns, sometimes along meninges within the cortical sulci over the cerebral convexities and in the sylvian fissures. These findings are better seen at contrast enhanced MRI than CT. This appearance is nonspecific and has a wide differential diagnosis that includes meningitis from other infective agents; non infective inflammatory diseases such as sarcoidosis, patchy meningitis; and neoplastic causes, both primary and secondary. In subtle cases or milder and initial stages a non specific faint hyperintensity in the region of cortical sulci on FLAIR may be be the only finding.
Common complication of tuberculous meningitis include:
A) communicating hydrocephalus, caused by blockage of the basal cisterns or arachnoid granulations by inflammatory exudates.
B) Occasionally, non-communicating hydrocephalus occurs due to the mass effect of a tuberculoma particularly at aqueduct or foramen of monro.
C) Vasculitis induced Infarcts, also a common complication, in ~ 30% of patients, mostly within the basal ganglia, resulting from vasculitis of perforators, rarely direct vascular compression. Carries bad prognosis and seen multi drug resistant cases.
D) Cranial nerve involvement , occurs in 17%–70% of cases, most commonly affecting the second, third, fourth, and seventh cranial nerves. Seen as abnormal enhancement along the nerve.

Parenchymal Tuberculosis
Tuberculoma (tuberculous granuloma), the most common CNS parenchymal lesion of tuberculosis.
This lesion may be solitary, multiple, multi locular or military.
May be seen anywhere within the brain parenchyma, most commonly frontal and parietal lobes.
Tuberculomas can exist in conjunction with tuberculous meningitis, although not a consistent combination.
At CT, tuberculomas appear as round or lobulated lesion with low or high attenuation, homogeneous or ring enhancement, irregular walls of varying thickness.  One-third of patients demonstrate the “target sign” (ie, central calcification or punctate enhancement with surrounding hypoattenuation and ring enhancement). This finding is suggestive of, but not pathognomonic for, tuberculosis.
The MR imaging findings depend on whether the tuberculoma is caseating, and if so, whether the center is liquid or solid. It is thought that there is a progression from noncaseating to caseating and then from a solid to a liquid center. A noncaseating tuberculoma is hypointense relative to gray matter on T1-weighted images and hyperintense on T2-weighted images, with homogeneous gadolinium enhancement.
Caseating tuberculomas with a solid center are isointense to hypointense on both T1- and T2-weighted MR images. They usually have a variable amount of surrounding edema, which is hyperintense on T2-weighted images. Caseating tuberculomas with a liquid center are hypointense on T1-weighted images and centrally hyperintense on T2-weighted images, with a peripheral hypointense rim on T2-weighted images that represents the capsule. Rim enhancement is usually seen at gadolinium-enhanced MR imaging.
Calcified tuberculoma or tubercular granuloma, after treatment, tuberculomas can completely resolve; however, calcification is seen in up to one-fourth of cases and is identified most clearly at CT as faint to dense nodular calcification with or without perilesional odema.
Miliary CNS tuberculosis, usually associated with tuberculous meningitis, pathogenetic relationship is suspected. At MR imaging appears as multiple tiny (<2-mm), hyperintense T2 foci with nodular or ring enhancement.
Tuberculous abscesses, are rarely seen and can be similar in appearance to liquid-centered caseating tuberculomas, although they tend to be larger and are more often multiloculated. At CT, these abscesses appear as hypoattenuating lesions with surrounding edema, mass effect, and peripheral geographic enhancement.
Tuberculous cerebritis, occurs very rarely.

Spinal tuberculous Meningitis
The MRI is must for imaging. Findings ranges from CSF loculation, matting of the nerve roots of cauda equina or patchy dural or cord enhancement. Chronic lesions may not enhance. Syringomyelia as a complication of arachnoiditis.


Image gallery of CNS TB:

Axial FLAIR show effacement of cortical sulci in dependent portions of brain with hyperintensity in the region of cortical sulci, needs Csf analysis to rule out meningitis.

Effacement of cortical sulci in dependent portions of brain with hyperintensity in the region of cortical sulci.




CT study showing hyper dense basal exudates with hydrocephalus and peri ventricular ooze of Csf.









MRI Contrast enhanced T1w images showing enhancing basal exudates with hydrocephalus.







MRI Contrast enhanced T1w images showing diffuse leptomeningeal enhancement with hydrocephalus and cerebral edema.

A ring enhancing tuberculoma.

Miliary tuberculosis








A dense nodular calcified granuloma with mild perilesional odema.

Tubercular abscess with multi locular ring enhancement.

A known case of tubercular meningitis with Vasculitis on MR Angio and recent vasculitis induced infarcts.

Sulcal hyperintensity on FLAIR

• FLAIR, Fluid Attenuated Inversion Recovery Sequence sequence has become a routine part of MRI studies of the brain; rather it has become the most commonly used sequence in MRI brain studies. In some institution like ours it is performed as a screening study for brain in cases of emergencies and non affordable patient.
• An inversion recovery pulse to null the signal from CSF and a long echo time to produce a heavily T2-weighted sequence. Produces images highly sensitive to T2-weighted prolongation in tissue but minus the Csf. Improves detection of lesions within the subarachnoid space and brain parenchyma, particularly the lesions located near the brain–CSF interface.
• When disease occurs within the subarachnoid space, the relaxation time of CSF is altered, result in hyperintensity of the CSF or subarachnoid space during the FLAIR sequence. Commonly seen in dependent portions of brain in parieto occipital region with effacement of cortical sulci, an alternative term cerebral odema can be used to describe this associated finding.

• Most common causes of this non specific diffuse hyperintensity along sulcal space is meningitis and subarachnoid hemorrhage (SAH).
• In meningitis and SAH both the  higher protein content and cellular concentrations causes an offset in the null point of CSF inversion times, resulting in increased T2-weighted prolongation.
• In massive SAH or obvious Meningitis with exudates diagnosis may not be a problem but in subtle cases, results of both in vivo and in vitro studies have suggested that FLAIR imaging is more sensitive than CT in the evaluation of these milder and subtle form of acute SAH and meningeal inflammation in which cases where CT may show only mild effacement of cortical sulci. Differentiation between the two is difficult most of time and is out of imaging consecus. Contrast enhanced T1 or Flair may help out by demonstrating leptomeningeal enhancement in meningitis.
• Always keep in mind other, less common cause of subarachnoid space FLAIR hyperintensity is artifactual. In my institution one patient was advised brain axial FLAIR and sagittal T2 cervical spine screening. First brain screening was performed, which was showing similar abnormal diffuse non specific hyperintensity along sulci spaces and basal cisterns. Cervical spine screening performed and axial Flair repeated again. It is strange to mention that this time axial flair screening was absolutely normal. I had two such incidences. After discussion with my technician i came to conclusion that this was artifactual as some changes were done by him in hurry in TR TE during the study.
• Patient intubated and on inhaled O2 can show similar abnormal diffuse hyper intensity in the region of cortical sulci and basal cisterns due to para magnetic effect of dissolved oxygen. 

Conclusion: Most of the time an associated finding may suggest the cause of the subarachnoid space hyperintensity on FLAIR. But in cases of milder form, diffuse distribution and a lack of ancillary findings often make this finding nonspecific and may require clinical correlation and CSF analysis. It’s better to mention the finding and suggest csf analysis. Commonest causes include meningitis and SAH.
Intubated patient on inhaled O2 can show similar picture due to para magnetic effect of dissolved oxygen.


To read more about effect of inhaled oxygen on FLAIR Click here

Streak artifacts CT

Occurs in CT

Distortions or errors in the image due to presence or movements of objects of very high density, like metallic clip and coil used for aneurysms, metallic implants and contrast media.

Seen as radiating dense white Streaks.

Effects:

Deteriorates image quality.

Subject information is lost

Pathological details lost.

Solutions :

Remove the offending object if possible.

Use a smoothing algorithm. e.g. Standard algorithm.

Radiating white streaks in right para sellar region due to metallic coil in situ used for right MCA aneurysm. 

MRI is strictly contraindicated.

Intracranial calcifications

Causes include physiological as well as pathological.
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.
Noncontrast-enhanced CT of the head is the preferred imaging modality over MRI. MRI is quite risky may miss faint calcification.
Causes: 
Physiologic calcification
Very common associated with aging , commonly seen in the basal ganglia, pineal gland, falx, tentorium, arachnoid granulations, choroid plexus and the cerebellum. Never clinically significant.
1. Basal ganglionic calcification: bilateral, faint, located within the globus pallidus, less commonly caudate nucleus and the putamen, very common in middle-aged individuals and the elderly.

Any calcification other than globus pallidi and before age of 10 is abnormal and should be investigated for underlying metabolic disorders as in this case.

2. Pineal calcification: seen in approximately 40% of normal people by the age of 20 years and usually less than 1 cm in diameter. Larger calcifications should raise concerns for underlying tumor.

3. Dural calcifications: Very common in older age groups and are usually located in the falx or the tentorium, usually few. Presence of multiple and extensive dural calcifications or dural calcification in children should raise the suspicion of underlying pathology.

4. choroid plexus calcification: 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. Commonly seen in atrium of lateral ventricles uncommonly in fourth ventricle.

5. Partial volume averaging at the base of skull: apparent appearance due to partial inclusion of bone in the section due to unevenness of bony floor of bony calvarium.

6. Finally, physiologic calcifications can be seen in the cerebellum, with the dentate nucleus being the most common site.
7. Gaint arachnoid granulations, along the transverse and sigmoid sinuses, are also calcified in middle-aged and older people.

Congenital disorders/phakomatoses
The phakomatoses are a group of hereditary disorders. Calcifications commonly described in tuberous sclerosis and Sturge-Weber syndrome but can also be seen in neurofibromatosis and basal-cell nevus syndrome.
1. In tuberous sclerosis, Calcified subependymal nodules along the lateral ventricle and  caudo thalamic groove. Associated with cortical hamartomas  which may show calcification. 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.

2. In Sturge-Weber, Gyriform cortical calcifications with ipsilateal atrophy and enlarged choroid plexus.

3. In neurofibromatosis type 2 (NF2) tumeral calcification of like meningiomas and nontumoral calcifications like disproportionate calcification of choroid plexus in the lateral ventricles and nodular calcifications of the cerebellum being most commonly observed.

4. In basal-cell nevus syndrome early dural calcifications are a common manifestation involve the falx, 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.

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, an independent risk factor for stroke. The carotid siphon is the most commonly affected vessel, while calcifications in the anterior and middle cerebral arteries and the vertebrobasilar system are less common.

Calcification patterns associated with vascular pathology such as AVM nidus, aneurysms, cavernoma and capillary talengictesia.

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 infections result in peri-ventricular and subependymal calcifications. Interestingly, calcifications in patients infected with toxoplasmosis may resolve after treatment.
Congenital HIV infection is associated with periventricular frontal white-matter and cerebellar calcifications.
Congenital herpes (HSV-2) infection is associated with thalamic, periventricular, and punctate cortical or extensive gyral calcifications.

Acquired infections
Cysticercosis, tuberculosis, HIV and cryptococcus are the most common acquired intracranial infections typically associated with calcifications.
In cysticercosis 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; meningeal calcifications are much less common.

HIV encephalitis is associated with basal ganglia calcification.
Cryptococcus affects immunocompromised patients and calcifications can be seen in both the brain parenchyma and the leptomeninges.

Inflammatory lesions
Sarcoidosis involves the leptomeninges, 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 associated with cerebral calcifications in the basal ganglia, thalamus, cerebellum and centrum semiovale.

Tumors
Commonly calcified intracranial tumors include the oligodendrogliomas, low-grade astrocytomas, craniopharyngiomas, meningiomas, pineal gland tumors and the ependymomas.
In some instances, the presence and pattern of calcification can be essentially pathognomonic as in the case of oligodendrogliomas and craniopharyngiomas.
The presence or absence of calcifications is not related to the benign or malignant nature of the tumor.
Craniopharyngiomas show curvilinear calcification.
Dermoid and epidermoid tumors show peripheral stippled calcification, teratomas show internal calcification.
Pituitary adenomas do not calcify frequently.
Pericallosal and interhemispheric lipoma with calcification.

Endocrine/metabolic/idiopathic
Metabolic disorders affecting the calcium homeostasis 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, thalami, subcortical white matter and dentate nuclei calcifications have been described.
Chronic renal failure and secondary hyperparathyroidism,
Hypoparathyroidism,
Pseudo hypoparathyroidism.
Hypothyroidism is also associated with basal ganglia and cerebellar calcifications.
Rare idiopathic disorders such as Fahr disease.

Dystrophic calcifications
Seen as a chronic sequelae of trauma, surgery, ischemia and radiation therapy, often associated with encephalomalacia and gliosis.
Post traumatic calcifications have been described in the capsule surrounding both chronic subdural and epidural hematomas.
Radiation–therapy- and chemotherapy-related calcifications are of three main types.
• 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.

Reference:  applied radiology; Intracranial calcifications; Erini Makariou, MD, and Athos D. Patsalides, MD