Hydatid cysts brain

A 34 y o male with headache, nausea and vomiting.
Here is his MRI Brain, Axial T2, T1, FLAIR, Diffusion, Post contrast T1w images with MR Spectroscopy.

This MRI study of Brain shows:
Multiple intra axial round to ovoid unilocular cystic signal intensity focal lesions in supra tentorium as well as posterior fossa.
Fluid content of cyst is not very clear as it is hyperintense on FLAIR due to incomplete signal suppression of fluid, debris is seen in dependent portions.
The lesion in posterior fossa show no perilesional odema, lesions in parietal regions show mild odema underneath the lesion (may indicate an associated inflammation or a superadded infection).
None show restricted diffusion on DW images.
No significant mass effect.
Thin uniform thickness wall, non enhancing on post contrast T1w images.
On single voxel MR Spectroscopy at short TE of  35ms from right to left;
At 1.3 ppm - sharp doublets of lactate.
At 2.01ppm - no peak of NAA.
At 3.03ppm - no peak of Creatinine.
At 3.2ppm - no peak of Choline.

Imaging diagnosis : Hydatid cysts. 

Follow up not available.


CEREBRAL HYDATID 

Echinococcus (hydatid disease) affecting the CNS, is caused by E granulosis most commonly and E multilocularis.
Dogs or other carnivores are definitive hosts.
Sheep or cattle are intermediate hosts.
Humans are secondarily infected by ingestion of food or water contaminated with parasite eggs.
Parasite from GI tract to portal system, lymphatics.
Infection usually occurs in liver and lungs.

Typical imaging findings are large uni or multilocular cyst, isodense to CSF on CT and MRI. No edema and enhancement is typical. Fine peripheral enhancement may be seen on MRI. Calcification rare.

DDs
Neoplasm
Primary or metastatic (primary often known)
Thick, irregular margin enhancement typical.
Abscess
T2 hypointense rim and restricted diffusion is typical.
Perilesional odema.
Ring-enhancement.
Porencephalic cyst
Encephalomalacia +/- surrounding gliosis
Typically communicates with ventricle

Clinical presentation
Occur at all ages but commonly affect children and young adults.
Signs and symptoms depend up on location of the lesion.
Lesion develops slowly over many years. May get complicated by rupture, hemorrhage, secondary infection

Treatment
Variable, ranges from oral therapy to lesion resection.

Subdural Empyema

CT and MRI Axial T2 and Diffusion study of brain show diffuse cerebral edema with mild ventriculomegaly. 

Right side mastoiditis.

A thin layer of subdural collection along tentorium and interhemispheric fissure with restricted diffusion is very typical of a Subdural Empyema.

Related post : Subdural-abscess

EMPYEMA 

Syn: Subdural (SDE) or Epidural (EDE) Abscess. 

An extra axial localised collection of pus in sudural or epidural space or both.

SDE is more common than EDE.

Location: 

SDE more common in Supra tenotrium ( Cerebral convexity > interhemispheric fissure > tentorium) than Infratentorium (Cp angle > Cerebellar convexity) 

EDE in Supra tentorium common in Frontal region. 

Imaging findings:

Collection is extra axial cresentic shaped if SD and bi convex shaped if ED.

Density on CT and signal intensity on MR vary depending up on its density and protein content. 

Strong peripheral enhancement on post contrast is must. 

Restricted diffusion on MRI Diffusion is typical and is helpful to rule out other DDs like sub dural hygroma and effusion. 

Clinical Presentation:

Can occur at any age, No gender predominence. 

Often present with headache and fever. May show signs of meningitis. 

Etiology: 

An mastoid or sinus infection present in more than 75%.

Can be a complication of trauma or neurosurgical procedure. 

Prognosis: 

Progress rapidly, fulminant course, a neurosurgical emergency.

Complications and bad prognosis more common in SDE than EDE are CVT, focal cerebritis, Parenchymal abscess, meningitis, Hydrocephalus. Reason is in EDE the tough dura limits the collection and act as barrier between infection and brain. 

Mortality is 10-15%. 

Diagnosis solely based on imaging.

Lumbar puncture can be fatal. Csf examination can be normal. 

Treatment:

Mainly surgical drainage by wide craniotomy followed by patching. 

IV Antibiotics. 

MRI Artifacts : Magic Angle Effect

MRI Sag STIR
An artifactual T2 bright signal seen in tendons and ligaments that are oriented at about a 55 degree angle to the main magnetic field, not to be mistaken for tear.

Signal from water molecules associated with the tendon collagen fibers not normally seen because of dipolar interactions that result in very short T2 Times. At an angle of about 55 degrees to the main magnetic field, the dipolar interactions become zero, resulting in an increase of the T2 Times about 100 fold. This results in signal being visible in tendons. A bright signal from this artifact is commonly seen in the rotator cuff and distal patellar tendon.
Reference : http://www.mritutor.org/mritutor/magica.htm

Medulloblastoma

An 18 yo male with nausea and vomiting.
Here is his Non contrast CT Brain, MRI Brain Axial T1, T2, FLAIR, Diffusion, Post contrast T1w images at the level of posterior fossa with single voxel MR Spectroscopy at TE of 35 ms.

This CT and MRI study of Brain shows:
A well circumscribed ovoid intra ventricular space occupying mass completely occupying and expanding fourth ventricle, leading to mild obstructive hydrocephalus. 

Lesion is solid, hyper dense on CT with spotty calcification at the center.
Signals isointense to cortical gray matter on T1 and FLAIR, slightly hyperintense on T2w images. No cystic component. No marked areas of necrosis. Restricted diffusion on MRI Dw images. Lesion is lobulated, mild heterogeneous enhancement on post contrast T1.
On MR Spectroscopy, no peak of NAA at 2.01ppm, no peak of creatine at 3.02 with long sharp peak of raised choline at 3.2ppm.

Here are MRI Axial T1, T2 and FLAIR images with post contrast T1w images of same patient at the level of lateral ventricles shows multiple discrete enhancing nodules along ependymal lining of lateral ventricles, signal of nodules on MRI are same as that of the posterior fossa mass with same restricted diffusion.

Imaging diagnosis : Medulloblastoma with Csf dissemination. 

Similar post:

Medulloblastoma MR Spectroscopy
Lateral origin medullobastoma


MEDULLOBLASTOMA

Syn: MB, Posterior fossa PNET, PNET – MB,
A highly cellular embryonal cell tumor.
Age group : common in children, ~75% diagnosed by 10 years.
3 times more common in males.

Location:
Intraventricular – 4th ventricular roof is a typical and most common location. A most common posterior fossa tumour in children.
Lateral origin – Cerebellar hemisphere is an atypical location common in older children and adults.

Size vary, average size ranges between 3- 5cm at the time of presentation.
On Non contrast CT, solid 4th ventricle mass, hyperdense, calcifcaiton seen in ~20% cases, small intra tumoural cysts, necrosis in ~50% cases.
On MR signal on T1 iso - hypo intense to cortical grey matter on T1 , iso – hyperintense on T2w and FLAIR. High signal on diffusion attributed to its dense, highly cellular nature.
An associated Obstructive hydrocephalus is common seen in ~ 95% cases.
Usually mild to moderate and homogenous enhancement, may show patchy heterogeneous enhancement due to areas of necrosis.
On MR Spectroscopy, NAA reduced or absent as it’s a non neuronal tumour, raised choline.

Dural AV Malformation / Fistula MRI

MRI Brain Axial FLAIR and coronal T2w images show an extra axial nodular T2 flow voids in right parasellar region, flow related signals on 3D TOF Noncontrast MR Angiography suggestive of a high flow vascular malformation. No direct communication with adjacent right ICA rules out ICA Aneurysm.
It seems to be a Dural Arterio Venous Malformation / Fistula, finding is noted incidentally as pt actually presented for a recent infarct involving cranial portion of right cerebellar hemisphere in superior cerebellar artery territory. 

Bilateral ICA aneurysms MR Angio

This MRI study of Brain Axial T2w images shows:
A right para sellar and a left supra sellar ovoid well circumscribed lesions with T2 flow voids in relation of ICAs, show flow related signals on 3 D TOF Non contrast MR Angiography suggestive of a right ICA cavernous portion and a left ICA supra clinoid portion aneurysm. 

When unilateral ICA aneurysm seen equally distributed on either side. When involve bilateral ICA called mirror aneurysms.

Aggressive Hemangioma MRI Spine

A 55 yo female with compressive myelopathy clinically.

Findings: 

D2 vertebral body and adjacent posterior elements show an abnormal altered marrow signals, heterogeneously hyper intense on T2 and STIR with low signal intensity vertical striations on sagittal sections, multiple punctate low signal intensity dots on Axial T2w sections so called as 'Polka dot' appearance corresponds to coarse, thickened vertical trabeculae characteristic of Spinal Osseous Hemangioma.
An associated anterior epidural lentiform shaped soft tissue causing canal stenosis, anterior displacement of cord with significant cord compression.

Imaging wise diagnosis : Aggressive vertebral Hemangioma.

HISTOPATHOLOGY REPORT

Gross Appearance : The specimen consists of grey brown soft and largely bony fragments together measuring ~ 25x14mm. Representative sections are submitted for processing after de calcifying bone.

Microscopy : A benign neoplasm composed of vascular tubes or spaces lined by endothelium and many containing blood. The interstitial tissue contains a couple of spicules or trabeculae of bone.

Histopathological Diagnosis : Spinal Intraosseous Hemangioma.

Vertebral body hemangioma are usually benign looking and asymptomatic.
Rarely aggressive and pt may present with cord compression due to an associated epidural soft tissue as in this case.

Similar case : Spinal-epidural-lesion-causing-cord compression

Cystic pituitary adenoma

A young male came for evaluation of visual field deficit. Pt was clinically stable.

This MRI study of Brain shows: 

MRI sagittal T1 and T2 w images show a sellar supra sellar oblonged cystic mass.
Cyst is slightly hyper intense than Csf on T1 and iso intense on FLAIR due to lack of signal suppression of fluid implies to thick viscous content of cyst. Thick profusely enhancing wall around cyst on Post contrast T1w images.
No solid component or multilocularity of cyst.
T1 bright normal posterior lobe of pituitary seen stretched along posterior wall of cyst on sagittal non contrast T1w images. Pituitary gland not seen separately in hypophyseal fossa. Pituitary stalk is seen ending at the top of cyst. Supra sellar anatomy distorted. Optic nerve and chiasma compressed.

Imgingwise DDs: Cystic pituitary adenoma more likely than Rathke’s cleft cyst (Thick profusely enhancing wall around cyst goes against Rathke’s cleft cyst).

Transnasal Transphenoid approach attempted.
Histopathology report : Pituitary Adenoma with Necrosis. 

Invasive macroadenoma

This MRI study of brain shows:

A well demarcated ovoid soft tissue signal intensity mass confined to sella seems to be the enlarged pituitary gland itself as pituitary gland is not seen separately in hypophyseal fossa, mild to moderate enhancement on post contrast T1. Both the ICAs are encased. Abnormal marrow signals involving clivus with erosions of floor of hypophyseal fossa. Sphenoid sinus show marked mucosal thickening and soft tissue. No significant mass effect on supra sellar anatomy.

Imagingwise diagnosis : Invasive / Aggressive Macroadenoma.

Tran sphenoid scopy and biopsy attempted, histopathology reports Macroadenoma.

All Sellar masses are not Macroadenoma

This MRI study of Brain shows:
A well circumscribed sellar supra sellar mass isointense on T1 as well as T2 images.
On post contrast images mass show homogenous enhancement, slightly lesser than that of normal profusely enhancing pituitary which is seen separately at the floor of hypophyseal fossa, rules out Macroadenoma, a focal dural tailing is seen anterior to the mass.
Significant mass effect over pituitary stalk and optic chiasma. ICAs are on etiher side of mass, not encased or invaded.

Imaging diagnosis : Sellar meningioma. 

Histopathology: Meningioma.

Colloid cyst MRI

COLLOID CYST 

Syn: paraphyseal cyst.
A well circumscribed round to ovoid solitary unilocular mucine containing third ventricular cyst.

CC contributes to 0.5-1.0% primary brain tumors and 15-20% intra ventricular masses.

Location is a diagnostic clue, more than 90% occur at Antero Superior corner of third ventricle at foramen Monro. In less than 1% of cases other sites are lateral ventricle and fourth ventricle.
Size variable from few mm to 3cm.
Density on CT and signals on MRI variable.

CT
Density correlates inversely with hydration state.
2/3rd are hyperdense.
1/3rd are iso to hypodense.
Usually doesn't enhance.
MRI
Signal on T1W images correlates with cholesterol concentration.
2/3rd are hyperintense.
1/3rd are isointense.
Signal on T2W images correlates with water content.
Majority isointense to brain on T2WI, Hypointense cysts are uncommon indicate high viscosity of cyst.
Hyper intense on FLAIR due to failure of signal suppression owing to its mucin content.
No restricted diffusion on DWI.
Usually doesn't enhance on post contrast T1.

Histopathology
CC develop from embryonic endoderm, not neuroectoderm similar to other foregut-derived cysts like neurenteric, Rathke cleft cyst. Ectopic endodermal elements migrate into velum interpositum. Contents accumulate from mucinous secretions, desquamated epithelial cells.
Microscopic Features are outer wall composed of thin fibrous capsule. Inner lining composed of simple or pseudostratified epithelium, interspersed goblet cells, scattered ciliated cells. Rests on thin connective tissue layer.
Cyst contents is PAS + gelatinous ("colloid") material, variable viscosity, +/- Necrotic leukocytes, cholesterol clefts.
Immunohistochemistry shows +/- Epithelial antigen reactivity (cytokeratins, EMA)
Electron microscopy, resembles mature respiratory epithelium, Non-ciliated or tall columnar cells, Basal cells contain dense core vesicles.

Clinical presentation
~50%  asymptomatic discovered incidentally.
Headache is most common symptom.
Less common are nausea, vomiting, memory loss, altered personality, gait disturbance, visual changes.
Acute foramen of Monro obstruction may lead to rapid onset hydrocephalus.

Age of presentation is 3rd-4th decade. Peak age is 40 years. Rare in children. M = F

Presence of growth, rate of growth and development of CSF obstruction varies.
90% stable or stop enlarging if diagnosed at older age, cyst is smaller in size and already Hyperdense on NECT, hypointense on T2w MRI.

Treatment
Requires no treatment if asymptomatic except close follow up.
Complete surgical resection is treatment of choice.
Image-guided endoscopic approach increasingly common.
Recurrence if resection is incomplete.

Stereotactic aspiration is difficult if content is extremely viscous / solid. Imaging features that may predict difficulty with percutaneous therapy are if its Hyperdense on CT and hypointense on MRI T2WI suggests high viscosity of the cyst.

Reference : Osborn Diagnostic imaging.

Invasive skull base lesion MRI

A 55 yo male with right side III, IV and VI CN nerve palsy. Non diabetic.
Here is his MRI Brain, Axial T2, FLAIR, T1w images with single voxel MR Spectroscopy. PC T1w images not available.

This MRI study of Brain shows:

A lobulated soft tissue signal intensity well circumscribed but locally invasive mass in right parasellar region, signals are hypo intense on T2w images with T2 hyperintense marked perilesional vasogenic odema in adjacent right temporal lobe. Right side ICA encased. Right side cavernous sinus obliterated explains involvement of CNs traversing through the right cavernous sinus. Destruction of floor of right middle cranial fossa near sphenoid sinus with a similar signal intensity soft tissue occupying right half of sphenoid sinus, rest of the sphenoid sinus show marked mucosal thickening.

On single voxel MR Spectroscopy, peak of lactate at 1.3ppm and raised choline at 3.02. Absent peaks of NAA and Creatinine implies to non Glial origin of tissue. 

Imaging wise possible DDs:

Locally invasive skull base Neoplasm.

Aggressive fungal infection.

Histopathology : Aggressive Fungal infection.

ICA Aneurysm MR Angio

 
Axial T2 and FLAIR images at the level of sella show a solitary ovoid left parasellar well circumscribed lesion with mixed signals, show flow related signals on 3D TOF Noncontrast MR Angiography, as a saccular outpouching from left intra cranial ICA supraclinoid portion is a an Aneurym.
Mixed signals instead of flow void in the outpouching on T2w images may be due to its partial thrombosis.

Arachnoid cyst MRI

A 32 y o male with left hemi facial pain for last 1 year. 

Here is his MRI Brain Axial FLAIR and Diffusion.

This MRI study of Brain shows a sharply demarcated left Cp angle cystic lesion. 

Extra axial, not communicating with ventricular system.
Isointense to csf, complete suppression of fluid signal on FLAIR. No septations or loculations.
No restricted diffusion on Dw images.
An associated hypoplastic left cerebellar hemisphere. No gliosis in adjacent brain parenchyma. No volume loss.
Mass effect is mild, decently displaces adjacent vessels and nerves without encasement. Left trigeminal nerve is stretched may be the cause of left hemi facial pain. Left 7-8th CN complex mildly displaced. No significant mass effect fourth ventricle to cause obstructive hydrocephalus.
Non enhancing on post contrast.

Imaging diagnosis : Left Cp angle Arachnoid Cyst.

Needs to be differentiated from its closest DDs;
1. Epidermoid cyst which typically shows restricted diffusion. Mass effect on adjacent parenchyma instead of hypoplasia, insinuates in cisternal spaces, encases nerves and vessels implies to its plasticity. Signal suppression on FLAIR may not be as complete as arachnoid cyst.
2. Porencephalic cyst show Gliosis in adjacent brain parenchyma and volume loss like ex vacuo dilatation of adjacent ventricle. May communicate with ventricular system. It’s a cortical area of Csf signals involves cortical grey white mater where as arachnoid is an extra axial lesion.
3. Neuroglial cyst is intra axial, rare, commonly seen in frontal lobes.

Related post :
Arachnoid-cyst parietal region - uncommon for site.
Epidermoid-vs-arachnoid-cyst

ARACHNOID CYST

AC belongs to a category of primary non neoplastic intracranial Cysts.
An intra arachnoid CSF-filled sac that does not communicate with ventricular system.
ACs contributes to ~ 1% of all intracranial masses and as incidental finding on imaging for seizure in ~ 2 % of cases.

Imaging wise diagnostic clue is sharply demarcated round/ovoid extra-axial cyst that follows CSF attenuation on CT or signal on all MRI pulse sequences. No restricted diffusion on DWI (vs Epidermoid cyst)

Most common location is middle cranial fossa (~50-60%), Cerebellopontine angle (~ 10%), Suprasellar arachnoid cyst (~10%), Cerebral convexity, quadrigeminal cistern (~10%)

Imaging findings
NECT: Hypodense with density same as that of Csf.
Calcification is not a feature.
Non enhancing on post contrast.
Hyperdense if intracyst hemorrhage present and is rare.
MRI
Iso intense to Csf on T1, T2w and FLAIR images. Complete signal suppression of FLAIR.
T2* GRE: No blooming unless hemorrhage present and is rare.
DWI, no restriction
T1 C+, doesn't enhance
MRA, cortical vessels displaced away from calvarium.

Associated abnormalities are scalloping of adjacent bony calvarium.
Hypoplastic adjacent part of brain for example temporal pole in case of middle cranial fossa ACs and Cerebellar hemisphere in cases of Posterior fossa ACs.

Pathogenesis 
AC is usually sporadic, non-syndromic, rarely familial.
Frontal, temporal embryonic meninges (endomeninx) fail to merge as sylvian fissure forms, remain separate, forming duplicated arachnoid. Proposed mechanism behind development of cyst are active fluid secretion by cyst wall, Slow distention by CSF pulsations, CSF accumulates by ball-valve mechanism.
Microscopic Features are wall consists of flattened but normal arachnoid cells. No inflammation, neoplastic cells.

Clinical presentation
Often asymptomatic and found incidentally
If symptomatic, symptoms vary with size, location of cyst. Headache, dizziness, sensorineural hearing loss, hemifacial spasm/tic.

ACs can be found at any age, 3-5 times more common in male.
Usually don't enlarge. If at all grows very slowly.

Treatment
Often requires no treatment.
May need endoscopic resection, Fenestration, Cystoperitoneal shunt.

Reference : Diagnostic imaging Osborn.

Epidermoid cyst MRI

A 35 yo female with left side Trigeminal Neuralgia clinically.
Here is her MRI Brain Axial T1 T2 FLAIR and Diffusion. 

This MRI study of Brain shows:
A lobulated extra axial left Cp angle cystic space occupying lesion.
Signals hypo intense on T1, hyper intense T2w images, hypo intense on Flair but signal suppression of fluid is not complete, not as clear as csf.
Restricted diffusion on Dw images. 

Cyst is insinuating in cisternal spaces. Significant mass effect, adjacent left cerebellar hemisphere, brain stem and fourth ventricle are compressed, left side trigeminal nerve stretched.
No obvious parenchymal invasion.
Contrast enhanced T1w images not available.

Imaging diagnosis : left Cp angle Epidermoid cyst.

Closest differential is Arachnoid cyst which shows complete signal suppression of fluid on FLAIR, as clear as csf, no restricted diffusion on Dw images, an associated hypoplasia of adjacent brain parenchyma, mass effect if any is mild and not significant as in this case.

Left retro mastoid craniotomy perfomed. Epidermoid cyst confirmed by intraoperative and histopathological findings.


EPIDERMOID CYST

Belongs to a category of primary non neoplastic intracranial Cysts.

Intracranial epidermoids are congenital inclusion cysts, arise from ectodermal inclusions during neural tube closure. Acquired develops as a result of trauma and is very very rare.

EC contributes to 0.2-1.8% of all primary intracranial tumors.
4-9 times more common than dermoid.
EC is a most common congenital intracranial tumor and is third most common CPA/lAC mass, after vestibular schwannoma, meningioma.
Associated abnormalities may be occipital / naso frontal dermal sinus tract.

EC is a lobulated, irregular, "cauliflower-like" cystic mass with "fronds", insinuates cisterns and encases nerves/vessels. Restricted diffusion on MRI DWI is a diagnostic clue.

Location
A. Intradural, in ~ 90% of cases, primarily in basal cisterns.
M/c is Cerebellopontine angle (40-50%), Fourth ventricle (~17%), Para sellar/middle cranial fossa (~10-15%), Rarely in cerebral hemispheres (~1.5%), Brain stem (rare), Intraventricular within tela choroidea of temporal horn, 3rd, or 4th ventricles.
B. Extradural, in ~ 10% , intradiploic to bony calvarium, spine.

Imaging findings
NECT
Often a round / lobulated mass, hypodense in more than 90% of cases, resembling a focal CSF density. In 10-25% an associated calcification noted.
"Dense" epidermoid – a rare variant secondary to hemorrhage, high protein, saponification of cyst debris to calcium soaps or iron-containing pigment.
Contrast enhancement is none. Very minimal enhancement may be present at its surface.
Intradiplioc epidermoid shows bony erosion with sharply corticated margins.

MRI
Signal on TlWI often slightly hyperintense to CSF.
Uncommonly hyperintense to brain ("white epidermoid") due to high triglycerides & unsaturated fatty acids
Uncommonly hypointense to CSF ("black epidermoid") due to presence of solid crystal cholesterol & keratin and lack of triglycerides & unsaturated fatty acids.
On T2WI, often isointense to slightly hyperintense to CSF.
Very rarely hypointense due to calcification, hydration, viscous secretions, iron pigments.
On FLAIR, hypo intense but slightly hyper intense than Csf due to incomplete suppression of fluid signals.
DWI, restricted diffusion is pathognomonic.
Post contrast Tl, usually none. Margin of cyst may show minimal enhancement.
MRS: lactate peaks.

Histopathology 
EC grows by progressive desquamation with conversion to keratin/cholesterol crystals.
Gross features are outer surface often has shiny, glistening "mother of pearl" appearance ("beautiful tumor"), Cyst filled with soft, waxy, or flaky material. Lobulated excrescences. Soft and pliable, conforms to shape of adjacent local structures/spaces. Insinuating growth pattern (extends through cisterns, surrounds and encases vessels/nerves.
Microscopic Features are Cyst wall shows internal layer of simple stratified cuboidal squamous epithelium covered by fibrous capsule and contents is solid crystalline cholesterol, keratinaceous debris. No dermal appendages.

Clinical Presentation
Age of presentation is usually between 20-60 y with peak at 40; no gender preponderance.
Symptoms depend on location, growth pattern.
Headache is most common.
Cp angle lesion present with 5, 7,8 CN neuropathy.
Cerebellar signs.
Increased intracranial pressure rare due to 4th ventricular compression.
Less commonly hypopituitarism, diabetes insipidus.
Seizures if in Sylvian fissure/temporal lobe.
May remain clinically silent. Grows slowly.
Chemical meningitis possible from content leakage.
Rare malignant degeneration into squamous cell carcinoma (SCCa) reported.

Treatment: 
Often surgical.
Complete resection often complicated by investment of local structures
Recurrence common if incompletely removed.
Subarachnoid dissemination of contents may occur during operative/postoperative course may cause chemical meningitis.
Rare malignant degeneration of resection bed into Sq Cell Ca reported, may occur years after surgical resection.

Reference: Diagnostic imaging Osborn.

Vascular loop at IAC

A 45 y o male with right side pulsatile tinnitus. 

Thin axial T2 images at the level of IAC show a vessel probably the right AICA forming a loop around right side 7th-8th nerve complex.
Vascular loops in the internal auditory canal may generate pulsatile tinnitus.
However significance to this finding to be given in proper clinical context only and the diagnosis of vascular compression syndrome should not be based solely on imaging findings.

Tuberous Sclerosis

5 y o child with seizures.

Here are non contrast CT and MRI Axial FLAIR images of Brain of same patient.

This CT and MRI study shows: 

Multiple sub ependymal nodular calcifications best seen on CT. 

Cortical tubers as cortical and sub cortical white matter small patchy T2 hyper intensities.

Mild Ventriculomegaly without any marked trapping.

Imaging diagnosis : Tuberous Sclerosis.

Advised follow up imaging for lesions at caudo thalamic groove.


Similar Case : Tuberous-sclerosis


TUBEROUS SCLEROSIS

Syn: Tuberous sclerosis complex (TSC), Bourneville-Pringle Syndrome.
A inherited tumor disorder with multi-organ Hamartomas.

In CNS characterized by Subependymal nodules, Subependymal giant cell astrocytoma, Cortical/subcortical tubers.
Abnormal differentiation/proliferation of germinal matrix cells, Migrational arrest of dysgenetic neurons appears to be the pathogenesis behind the lesions.
Histopathology and microscopic features are Balloon cells, Myelin loss, vacuolation and gliosis, Ectopic neurons.

Imaging 
CT and MRI both are equally sensitive but MRI often shows more number of lesions.
Subependymal nodules
Seen in ~ 98%. Commonest and specific site is caudothalamic groove followed by atrial and temporal lobe white matter.
~ 50% them shows an associated calcification best depicted on CT. calcification is often progressive after 1 yr.
30-80% of SEN shows mild enhancement on post contrast study, appreciated better on MRI than CT.
SEN at foramen of Monro needs close follow. If its enlarging it is equivalent to Subependymal giant cell astrocytoma (SGCA) and can cause obstructive hydrocephalus.
Subependymal giant cell astrocytoma (SGCA) 
Seen in ~15%.
Cortical/subcortical tubers, WM lesions
Seen in ~ 70-95% common in Fronto parietal followed by temporo occipital regions and Cerebellum.
Ill defined patchy hypodensites on CT +/- calcification.
Hypo intense on T1 hyper intense on T2 and FLAIR on MRI. No restricted diffusion. May show low signal intensity on T2*GRE if an associated calcification.
~12% cortical/subependymal tubers show faint enhancement on post contrast T1.
Cyst-like white matter lesions as focal lacune best seen on MRI T2w images, common in corona radiata.
An associated thickened cortex, enlarged gyri.
MRS: decreased NAA/Cr, increased ml/Cr in subcortical tubers, SENs.

Associated abnormalities
o Renal: Angiomyolipoma and cysts 40-80%
o Cardiac: Rhabdomyomas 50-65%; majority involute over time
o Lung: Cystic lymphangiomyomatosis/fibrosis
o Solid organs: Adenomas; leiomyomas
o Skin: Ash-leaf spots (majority) including scalp/hair; facial angiofibromas; shagreen patches 20-35% post pubertal
o Extremities: Subungual fibromas 15-20%; cystic bone lesions; undulating periosteal newbone formation
o Ocular: "Giant drusen" (50%)
o Dental pitting permanent teeth in most adults with TSC

DDs: 
Subependymal heterotopia : Isointense to GM, don't enhance or Ca++.
TORCH : Periventricular Ca++ , White matter lesions, Cortical dysplasia common with Cytomegalovirus (CMV).
Taylors dysplasia

Genetics
De novo = spontaneous mutation/germ-line mosaicism
Autosomal dominant, high but variable penetrance. Approximately 50% of TSC cases are inherited.

Clinical presentation

Classic clinical triad
1. Facial angiofibromas 90%;
2. Mental retardation 50-80%;
3. Seizures /  Epilepsy 80-90%

All three ("epiloia") seen in ~ 30% of cases.

More the number lesion ~ high the neurologic symptoms.
Diagnosed at any age.

First year of life commonly present with seizures, Infantile spasms like episodes.
Child present with Autistic-like behavior, mental retardation, seizures, or skin lesions.
Adult may present for first time due to a symptomatic SGCA.

Treatment
Treat seizures.
Resect isolated tubers if seizure focus or if able to identify seizure focus among many tubers.
SGCAs resected if obstructing foramen of Monro.

Reference : Diagnostic imaging Osborn.

Radiotherapy induced fatty marrow

A 67 y o female ,  a known case of Ca cervix with radiotherapy. Now complains of severe backache, radiating to lower limbs. Referred to MRI lumbar spine to rule out metastasis and cause of pain. 

Here is her MRI Lumber spine; Sagittal T1, T2 and STIR sequences. 

Diffuse homogeneously high marrow signals involving L5 and all sacral vertebral bodies on T1 and T2 w images with complete signal suppression on STIR implies to fatty marrow, it s a radiotherapy induced change, area of involvement corresponds to field of radiotherapy, should not be mistaken for neoplastic marrow infiltration.

A benign looking osseous haemangioma in D12 vertebral body with typical vertical striations and faint high signals on STIR again not be mistaken for metastasis.

Her cause of backache appears to be the degenerative changes marked at L4-5 with anterior subluxation of L4 off L5.


POST IRRADIATION VERTEBRAL MARROW

Transformation of normal cellular marrow into fatty marrow after therapeutic irradiation.
Radiation destroys hematopoietic elements which are highly radiosensitive.

Location and size corresponds to site of irradiation and extent of radiation field with sharp demarcation between irradiated vs. untreated adjacent normal marrow.
Marrow signals are often homogeneously hyper intense on T1. Heterogeneity may be due to residual or recurrent marrow disease.
Signals on T2WI are high to intermediate.
Signals on STIR variable depending up on timing of radiation.
In acute phase may signals are high on STIR indicating marrow edema and necrosis. Marrow odema is maximum at around ninth after irradiation, followed by subsequent gradual decrease in SI. After complete marrow reconverstion signals are homogenously low on STIR owing to signal suppression.

Marrow changes on MRI dependent on radiation dose, fractionation, and time elapsed after treatment.
No change in marrow SI with radiation dose of 1.25 Gy
Between 20-30 Gy dose, partial recovery occur between 2-9 years and return to normal marrow after long term follow-up ~ it takes 10 yr
At 50 Gy, Complete and irreversible changes occur. Persistent fatty marrow even after 9 years.

Fatty marrow seen on MRI as early as 2 weeks after therapeutic irradiation. ~ 90% will show fatty marrow after 2 months. Marrow reconversion in pediatric patients occur 11-30 months after radiation treatment, takes relatively longer time.

Usually asymptomatic and requires no treatment.
There may be Pain, Myelopathy and radiculopathy due to associated problems like compression fracture or tumor infiltration which needs to fixed accordingly.

Reference : Osborn Diagnostic imaging.

Idiopathic Cranial Hypertrophic Patchymengingitis

A 45 yo male with long standing headache.

Here is his MR Brain; Axial FLAIR images with Post contrast T1w images.

This MRI study of Brain show a focal vasogenic odema in right parietal sub cortical white matter.

Post contrast study performed which showed multi focal patchy nodular dural thickenings with abnormal enhancement. 

Imaging wise possibilities given were: Idiopathic hypertrophic patchymengingitis, Inflammatory pseudotumor, Tuberculosis. To give possibility of sarcoidosis  is relatively uncommon in India.

Pt’s  Xray chest was done to rule out pulmonary tuberculosis, lungs were clear.
Pt was given a trial of steroids.

Here is a follow up post contrast MRI study. 

Follow up MRI after 1 Month shows marked regression of lesions, relief from headache, goes in favor of Idiopathic Cranial Hypertrophic Patchymengingitis (ICHP).

HYPERTROPHIC PACHYMENINGITIS

Syn : Dural pseudotumor, Idiopathic cranial hypertrophic pachymeningitis (ICHP) is diffuse dural thickening without known etiology like neoplasm or infection.

Imaging wise best diagnostic clue is thickened enhancing meninges "turn the corner" under temporal lobes in continuous line from vertex on coronal sections.

CT often normal. May show hyper density along inter hemispheric dura and tentorial leaflets. Brain parenchyma show normal attenuation pattern.

MRI is the investigation of choice, shows dural thickening often bilateral follows inner calvarium, extends along falx, tentorium may extend into lACs, along spinal cord with enhancement on post contrast T1w.
Dural thickening has to be more than 2 mm, may be more than 1 cm.
Usually smooth, linear, diffusely thickened dura. Less commonly nodular, focal soft tissue mass like lesions.
Signals on MRI are often iso to hyper intense on T2w images. In cases of densely fibrosing pseudotumor may appear profoundly hypointense.
Invasive variety may show encroachment of dural venous sinus with abnormal MR Venogram, dural venous sinuses showing poor flow related signals.

Diffusely thickened dura is nonspecific finding and can be seen in a spectrum of following identifiable disorders:
- Congenital (mucopolysaccharidoses)
- Iatrogenic (surgery, shunti post-LP meningeal enhancement rare & should be diagnosis of exclusion)
- Trauma (chronic SDH)
- Spontaneous intracranial hypotension
- Infection (TB, HTLV- 1, indolent infections such as pseudomonas, syphilis, rhinoscleroma, fungal.
- Inflammatory (rheumatoid, sarcoid, Wegener, pseudotumor)
- Neoplasm (meningiomatosis, lymphoma, mets)
- Hematologic (monoclonal plasma cell hyperplasia, extramedullary hematopoiesis)
- Other causes fibrosing inflammatory pseudotumors, fibrosclerosis)
- Idiopathic.

Histopathological findings of ICHP
Meningeal fibrosis.
+/- Inflammatory cells (lymphocytes, plasma cells)
May have multinucleated giant cells
No bacteria, fungi, neoplastic cells.

DDs
Normal dural enhancement
- Thin less than 2 mm,
- Discontinuous, most prominent at convexity, less intense than cavernous sinus.
Chronic subdural hematoma
- May contain loculated foci of old hemorrhage
- May show calcification.
Neoplasm
- Lesion in adjacent bony calvarium common in metastasis
- Lymphoma often associated with systemic disease.
Infection/inflammation
- Sarcoid often has other lesions, diffuse non focal dural thickening is less common than focal dura based masses
- TB is meningitis lepto meningeal pattern of involvement is more common than patchy meningeal involvement.
- Sinus disease seen in Wegener, Rheumatoid arthritis, SLE, Sjogren
Intracranial hypotension
- Associated finding are sagging midbrain on sagittal sections with tonsillar herniation.
- Dural venous engorgement.
Dural sinus occlusion
- Engorgement of collateral venous channels may thicken dura

Clinical Presentation: 
Any age; peak 3rd-5th decades.
Most common complaint is Headache.
Cranial neuropathy: Progressive sensorineural hearing loss, hoarseness, optic neuropathy, Tolosa-Hunt syndrome.
Uncommonly seizures.

Prognosis and Treatment: 
Variable course.
Some are benign, require no treatment.
Specific diagnosis may require biopsy.
Corticosteroid therapy. Recurrence may occur with steroid tapering
Immunosuppressants (e.g., methotrexate, azathioprine)

Reference : Diagnostic imaging Osborn.

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Hypertrophic patchymeningitis
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