Intracranial hypotension MRI

A 45 yo male with headache and altered sensorium.
Here is CT and MRI study of brain axial T2w and sagittal T1w images.

This CT and MRI study of Brain shows:

Bilateral subdural collections, isodense on CT appears to be sub acute sub dural hematoma.
Both the lateral ventricles compressed and medialised.
Mid brain compressed and antero posteriorly elongated.
Brain stem sagging down on sag T1 with abnormal downward protrusion of cerebellar tonsils.

Based on above findings diagnosis of Intracranial Hypotension needs consideration clinically. 

Patient given head low showed partial clinical improvement.

Intracranial Hypotension

Syndrome of headache caused by reduced intracranial CSF pressure.
Reduction of intracranial pressure is due to reduction in Csf volume.
Clinically characterized by headache marked in upright posture - postural headache. May have isolated abducens nerve palsy, necks stiffness, hearing loss.
The condition may be spontaneous or secondary to lumbar puncture. Other cause includes neurosurgical procedure, dehydration, and trauma. Lumbar puncture is most common cause among all.

Possible imaging findings in Intracranial Hypotension
- Diffuse thickening of the pachymeninges with enhancement or
- Subdural effusion / hematoma in advanced cases.
- Engorgement of dural venous sinuses.
- Enlargement of the pituitary.
- Slit like lateral ventricles.
- Antero posterior elongation of mid brain.
- Sagging brain stem.
- Protrusion of cerebellar tonsils.

Classical triad : 
1 Brain stem sagging.
2 Dilatation of veins and dural sinuses.
3 Dural thickening with enhancement, subdural fluid collections.
....not expected in every case, absence of any one of them does not preclude the diagnosis.

Most of these findings are the result of vascular dilation to compensate for sudden depletion of Csf volume, the explanations are based on Monro Kellie hypothesis, which states that the sum of the volumes of intracranial blood, CSF, and brain tissue remain constant in an intact cranium. Accordingly increased intracranial blood volume compensates for acute loss of CSF. Dilation of the venous side of circulation contributes a lot due to its high compliance and capacitance.
Meningeal enhancement is thick, linear, without nodularity and involves the pachymeninges without evidence of involvement of the leptomeninges.
Dura matter, the innermost layer composed of fibroblasts with inter digitating processes that create spaces in between. Extravasation of fluid occur into this layer, in these spaces, in response to increased dural vasculature as the dura lacks blood brain barrier and tight junctions.These extravasations explains dural thickening as well as contrast extravasation and enhancement. Tight junctions in arachnoid and pia mater prevent the similar contrast accumulation, explaining enhancement is limited to the dura. Though it is a frequent finding, abnormal meningeal enhancement is not the rule as cases are reported which are still symptomatic but enhancement that resolved earlier where as in certain typical cases MR images never revealed enhancement at any stage of disease.
Sub dural effusions occur when the extravasation continue even after meningeal thickening and enhancement, to the point of fluid accumulation in the subdural space as supported by studies in which effusions were not seen in the absence of meningeal enhancement represent more advanced stage of the condition. These sub dural effusions are typically thin, crescentic, often bilateral.
Subdural hematoma occur when effusion get complicated with bleed in subdural space due to rupture of the bridging veins traversing sub dural space in response to traction by ongoing extravasation and effusion.
Descend of cerebellar tonsils with sagging of brain stem, an associated effacement of prepontine cistern, obliteration supra chiasmatic cistern with inferior displacement of the optic chiasm result from reduction of normal Csf buoyancy due to reduced csf volume and represent most advanced stage of disease and severe Csf volume depletion, occurs after all other compensatory mechanisms have exhausted.
Isolated 6th nerve palsy reported in considerable amount of cases. In fact it is the most common nerve among all to get affected due to its longer intracranial course. Often get encountered at inisura when there is sagging of mid brain with antero posterior elongation.
Engorgement of dural venous sinuses seen as enlarged and round dural venous sinuses which are normally triangular in shape on cross sections.
Pituitary enlargement reflects simple compensatory venous hyperaemia.
Regression in these imaging findings often parallels clinical improvement of these, reversal of pituitary enlargement occurs first.

Most important is after sincerely mentioning all the findings, one must mention or suggest about the condition of so called intra cranial hypotension in the report, a frequently misdiagnosed syndrome of headache caused by reduced intra cranial pressure to alarm clinician that sagging down brain stem and tonsillar desend is due to low intra cranial pressure and not secondary to raised intra cranial pressure due to bilateral sub dural hematoma. Craniotomy for evacuation of subdural hematoma or decompression should not be attempted.

Treatment: 
Aimed at restoring CSF volume by fluid replacement.
Bed res with head low.
Active leak, Lumbar or directed epidural blood patch.Intrathecal saline infusion.
If blood patch fails dural suturing, packing with muscle pledget, Gelfoam or fribrin glue.

Reference : Intracranial Hypotension Syndrome: A Comprehensive Review: Imaging Studies; Neurosurg Focus. 2003;15(6) © 2003 American Association of Neurological Surgeons.

Other similar cases:
intracranial-hypotension
post-lumbar-puncture-intracranial hypotension
post-lumbar-puncture-intracranial.hypotension
cvt-and-intracranial-hypotension

Canavan disease MR Spectroscopy

A 9 y o male with severe hypotonia, enlarged head size on clinical examination.
Here is MRI Brain with single voxel MRI Spectroscopy.
Axial T2w images with sag T1w image of Brain.
Single voxel MRI Spectroscopy performed with a 2x2cm voxel placed in left medial occipital white matter, 99% water supression achieved. Spectral waveform obtained at long TE of 144 ms.

MRI study of Brain shows:
Bilateral diffuse T2 hyper intensity involving cerebral cortical white matter, involvement of thalami and dentate nuclei.
Sub cortical U fibers are typically involved.
Mild diffuse cerebral cortical atrophy.
MR Spectroscopy shows a sharp and long peak of NAA at 2.02 ppm suggestive of marked elevation of NAA.

Imaging diagnosis : Canvan's disease.

CANAVAN DISEASE


Syn: Spongiform leukodystrophy.
Progressive autosomal-recessive leukodystrophy.
Genetics
ASPAgene at 17 pter-p13;
Ashkenazi descent: Glu285Ala =  Non-Ashkenazi descent: Ala305Glu.

Deficiency of aspartoacyclase > N-acetyl aspartic acid increase in brain and urine, NAA is neurotoxic > Vacuolization (spongy degeneration) of white matter.

Imaging wise diagnostic clue is diffuse confluent demyelination with early U-fiber involvement. 

CT
Diffuse decreased attenuation of cerebral white matter.
Reduced attenuation in globus pallidi and thalami.
MRI
T1WI: Hypointense signal throughout cerebral WM
T2WI : Subcortical U-fiber involvement, centripetal WM involvement. Thalamic and globi pallidi hyperintensity. Progressive cerebral cortical atrophy and cerebellar dentate nuclei involvement in late cases.
DWI: Restricted diffusion at affected sites.
Lack of enhancement on PC T1.
MRS:Marked increased NAA at long TE of 144 or 288.

DDs
- Alexander disease
Predilection for frontal WM. Macrocephaly +
- Metachromatic leukodystrophy
Butterfly pattern of hemispheric demyelination, spares U-fibers
- Pseudo-TORCH
Confluent cerebral and cerebellar demyelination. Basal ganglia, thalamic, and periventricular Ca++
- Pelizaeus-Merzbacher disease
Profound deficient myelin development.

Histopathologic Features
Edematous/gelatinous brain tissue, necrosis subcortical V-fibers.
Microscopic Features are spongiform degeneration of white matter. Loss of myelin sheath, sparing of axonal fibers.

Clinical Presentation
Three clinical variants: Congenital / Infantile / Juvenile.

Congenital (first few days of life): Early encephalopathy, rapid death.
Infantile (3-6 months) MOST COMMON: Hypotonia, lethargy, head lag, macrocephaly, seizures, spasticity, optic atrophy.
Juvenile (onset at 4-5 years): slower progression.

Age at the presentation, usually evident by four months of age.
No sex predilection.
Increased risk for Ashkenazijewish ethnicity.

Prognosis
Relentless, progressive neurodegenerative disorder.
Chronic vegetative state with autonomic crises. Death by the end of the first decade.
Age of onset predicts course of disease.

Treatment
Not currently available.
Gene therapy and acetate supplementation are under evaluation.

Reference: Diagnostic imaging Osborn.

Hallervorden Spatz syndrome

A 19 y o male with extra pyramidal motor impairment.

Here is non contrast CT Brain

MRI Brain Axial T1, T2, FLAIR and Diffusion.

Findings:
Axial CT study of brain normal.
Axial T1w images of brain are unremarkable.
T2 and FLAIR images show bilateral symmetrical T2 hyperintensity in the region of Globus pallidi with low signal intensity rim surrounding the T2 hyperintensity - 'Eye of tiger' appearance.

Imaging diagnosis : Hallervorden Spatz.

Hallervorden Spatz Syndrome

A rare condition.
Syn: HSS; Pantothenate Kinase- Associated Neurodegeneration (PKAN); neurodegeneration with
brain iron accumulation type 1 (NBIA type 1).
Neurodegeneration with brain iron accumulation (NBIA) is a new umbrella term for disorders of focal brain iron accumulation, includes former HSS, aceruloplasminemia, neuroferritinopathy and others.
HSS is a progressive neuro degenerative disorder characterized brain iron accumulation.

Imaging wise the diagnostic clue is "Eye-of-the-tiger" sign, a bilateral, symmetric T2 hyperintensity in globus pallidi surrounded by hypointensity. The ferritine bound iron deposition is responsible for T2 hypo intensity.

CT Findings: Normal or Hyperdense Globus Pallidi.
MRI (The best imaging tool) Findings:
• Tl WI: Variable (ferritin-bound iron has greater Tl shortening than hemosiderin-bound)
• T2WI and FLAIR : Eye-of the tiger appearance in Globus pallidi.
• T2* GRE: Low signal intensity "bloom" due to paramagnetic effect iron.
• T1 C+: No abnormal enhancement.
• MRS:  reduced NAA in GP implies to neuronal loss.

Lab findings: Normal serum and CSF iron levels.

Genetics:
o Autosomal recessive (50% sporadic)
o PKAN: PANK2 mutation on chromosome 20p12.3-p13.
Theory is PANK2 mutation > CoA deficiency > energy and lipid dyshomeostasis > production oxygen free radicals > phospholipid membrane destruction. Basal ganglia in that GB is esp more prone to oxidative damage because of high metabolic demands. Cysteine accumulation in GP secondary to decreased phosphopantothenate causes iron chelation and peroxidative cell membrane damage is a contributing factor.

Clinical presentation:
Dystonia (most common), other extrapyramidal signs/symptoms are dysarthria, rigidity, choreoathetosis.
Cognitive decline is frequent, dementia.
Pigmentary retinopathy 66%
Psychiatric and speech disturbances
Teenager with speech, psychiatric disturbance is classical. Majority present before age of 6 yrs.

Prognosis: 
Fatal;
Mean duration disease after symptom onset = 11 yrs

Treatment: 
No curative treatment.
Iron chelation ineffective.
Palliative treatment with Baclofen, trihexyphenidyl, stereotactic pallidotomy, Pantothenate (vit B5).

Reference: Diagnostic Imaging Brain, Anne G. Osborn.

Adrenoleukodystrophy MRI

A 10 y o male with learning disabilities. Poor hearing. 

Here is MRI Brain Axial T2w and Dw images. 

This MRI study of Brain shows T2 hyper intensity involving splenium of corpus callosum, adjacent peri trigonal white matter and along cortico spinal tract. Bilateral symmetrical involvement with restricted diffusion on Dw images.

Imaging diagnosis : Adrenoleukodystrophy.

ADRENOLEUKODYSTROPHY

Syn : X-linked adrenoleukodystrophy (X-ALD) a severe progressive form usually affecting pre-teen males.
An inherited disorder of peroxisome metabolism, there is defect in VLCFA importers leading to impaired Beta-oxidation of Very Long Chain Fatty Acids (VLCFA) which then accumulate in WM leading to brittle myelin.

Pathology 
VLCFA accumulate in all tissues of body
Symptomatic accumulation occurs in CNS myelin, adrenal cortex, Leydig cell testes.
Adrenal failure associated with skin bronzing.
Testes involvement associated with early androgenetic alopecia in adults.

Genetics
X-ALD: X-linked recessive, Xq28; mutations ABCDI gene.

Epidemiology
X-ALD and variants: 1 per 16,800 births in North America

Clinical Presentation
Most common signs/symptoms: Skin bronzing, behavioral difficulties, hearing problems
Pre-teen male (3-10 years): Behavioral, learning, gait, hearing, vision difficulties.
Diagnose of "Addison/adrenal insufficiency" (skin bronzing, nausea & vomiting, fatigue) may predate diagnose of X-ADL
Age: Pre-teen males.

Gender: Males in classic X-ALD. Female carrier.
predominates in North America and France.


Imaging wise diagnostic clue is Peri trigonal white matter demyelination. 
Pattern of involvement is confluent, bilateral symmetrical, typically posterior involvement. Frontal pattern involvement is rare.
Predominantly involves Splenium and adjacent Peri trigonal WM followed by Corticospinal tracts/fornix/commissural fibers/visual and auditory pathways. Typically spares subcortical U-fibers.
MRI is the investigation of choice shows confluent T2 hyper intensity with restricted diffusion. On PC T1w images, leading edge (intermediate zone) enhances. Contrast-enhancement and diffusion restriction strongly linked to progression of disease process.
MRS, increased NAA even in normal appearing White matter predicts progression; High Cho, myo-inositol (ml), lactate peaks between 0.9 and 2.4 ppm probably represent VLCFA macromolecules.

Staging, Grading or Classification Criteria : Loes' MRI scoring system
Severity score based upon location and extent of disease and atrophy
o Pattern 1: Parieto-occipital WM (rapid progression if contrast-enhancement present and very young)
o Pattern 2: Frontal WM (same as pattern 1)
o Pattern 3: Corticospinal tract (adults, slower progression)
o Pattern 4: Corticospinal tract and cerebellar WM (adolescents, slower progression)
o Pattern 5: Concomitant parieto-occipital and frontal WM (mainly childhood, extremely rapid)

Imagingwise DDs
Periventricular leukodystrophy / Leukomalacia shows Periventricular gliosis and volume loss following hypoxia of prematurity, hypoglycemia ; doesn't enhance on post contrast T1.
Alexander disease
Enhances, but frontal predominance, not peri trigonal WM. Macrocephaly clinically.
White matter disease with lactate (WML)
Involves splenium, peri trigonal WM and corticospinal tracts, but doesn't enhance.
Metachromatic leukodystrophy
Involves fronto parietal white matter equally. Doesn't enhance.


Natural History & Prognosis
Progresses to spastic quadriparesis, blindness,deafness, vegetative state

Treatment
Vegetative state, death in 2-5 years without bone marrow transplantation.
Cholesterol-lowering drugs, dietary VLCFA restriction, glycerol trioleate/trierucate intake, plasmapheresis, interferon, immuno-ablation
Early bone marrow transplantation (BMT) stabilizes demyelination.


Reference : Osborn Diagnostic imaging.

Arterio Venous Malformation MRI

Clinically a young patient with right sided sudden onset focal neurological deficit. 

Here is his MRI Brain Axial T2w images with non contrast 3D TOF MR Angiogram of Brain.

This MRI study of Brain show a focal tightly packed cluster of serpigenous flow voids giving so called 'bag of black worms' appearance of an Arterio Venous Malformation in left medial occipital lobe and on surface of left temporal lobe. Left PCA and cortical branches from left MCA inferior division appears to be the feeder.

Related post : Arterio venous malformation


Arterio Venous Malformation (AVM)

A high flow vascular malformation with arterio venous shunting, no intervening capillary bed.

Imaging wise diagnostic clue is tightly packed mass of enlarged vascular channels.
CT:
Plain CT is insensitive for small aneurysms.
Contrast enhanced CT study is must. Mass of tightly packed iso to hyperdense serpentine vessels with strong enhancement on post contrast. Calcification seen in ~20-30%.
MRI:
Investigation of choice, typical imaging findings even on non contrast study. Most preferred sequence is T2w images.
A focal intra axial 'bag of black worms' due to flow voids on T2w images. Signal on T1w images varies with flow rate, direction, presence of hemorrhage and blood degradation products. Strong enhancement noted on post contrast T1w images. FLAIR images may show adjacent parenchymal hyper intensity due to an associated odema or Gliosis. Low signal intensity hemosderin staining on T2*GRE may be seen if hemorrhage. Dw images are often non contributory.
MR Angiography and Venogram to depict feeder and venous drainage.
DSA:
Digital Substraction Angiography is Gold standard, delineates internal angio architecture.
Depicts three components of AVMs - enlarged arteries, Nidus of tightly packed vessels, Draining veins (AV shunt with early appearance of contrast in enlarged veins).
In ~ 20-30% of cases AVM has dual arterial supply (Dural, Pial). Dural supply of AVM occurs through leptomeningeal anastomosis or transdural anastomoses with normal cortical arteries. Identification of transdural anastomoses is important as it decides treatment plan, embolisation vs surgery.

In CNS, AVMs may occur anywhere in Brain and Spinal cord.
In Brain, in ~85% are in supra tentorium and ~ 15% in posterior fossa.
In ~98% of cases are solitary and sporadic lesions. Rarely multiple AVMs, are usually syndromic.
Size is variable from few centimeters to Gaint occupying complete left hemi cranium.
Associated abnormalities are aneurysm on feeding artery 10-15%, intranidal"aneurysm in > 50%.

Vascular "steal" may cause ischemia in adjacent brain



Pathogenesis: 
AVMs have dysregulated angiogenesis, undergo continued vascular remodeling.
• Vascular endothelial growth factors (VEGFs), receptors mediate endothelial proliferation, migration
• Cytokine receptors mediate vascular maturation, remodeling.

Genetics: 
Sporadic AVMs have multiple up-, down-regulated genes. Homeobox genes such as Hox D3 and B3 involved in angiogenesis may malfunction.
Syndromic AVMs (2% of cases). Multiple AVMs in HHT 1 (endoglin gene mutation). Cerebrofacial arteriovenous metameric syndromes (CAMS) have orbit/maxillofacial + intracranial AVMs.

Histo pathology
Gross specimen is wedge-shaped, compact mass of tangled vessels.
Microscopic features have wide phenotypic spectrum
Feeding arteries usually enlarged but mature (may have some wall thickening)
Enlarged draining veins (may have associated varix, stenosis)
Nidus
• Conglomeration of numerous AV shunts ("micro AVFs")
• Thin-walled dysplastic vessels (no capillary bed)
• Disorganized collagen, variable muscularization
• Lack subendothelial support
• Loss of normal contractile properties
• No normal brain (may have some gliosis)
Perinidal capillary network (PDCN) -  a nidus surrounded by dilated capillaries in brain tissue 1-7 mm outside nidus border, larger than normal capillaries, connects both to nidus, feeding arteries/draining veins, surrounding narrowed brain vessels

Spetzler-Martin scale
Size
• Small <3 cm="1</p">• Medium 3-6 cm = 2
• Large > 6 cm = 3
Location
• In "noneloquent" area = 0
• If involves eloquent brain = 1
Venous drainage
• Superficial only = 0
• Deep = 1
Sum of above estimates surgical risk

Clinical Presentation
Most common signs/symptom is Headache with hemorrhage 50%, Seizure 25%, Focal neurologic deficit 20-25%
Often Young adult with spontaneous non traumatic ICH. M = F

Prognosis
All brain AVMs are potentially hazardous
Risk of first hemorrhage is lifelong, rises with age (2-4%/year, cumulative)
Vast majority will become symptomatic during patient's lifetime
Spontaneous obliteration rare < 1% of cases

Treatment
Embolization, stereotaxic radiosurgery, microvascular surgery

Reference: Osborn Diagnostic Imaging.

Diastematomyelia MRI

A congenital malformation of the spinal cord.
Results due to abnormal splitting of the notochord, possibly due to an obstacle between the endoderm and ectoderm encountered during migration. Most commonly seen in upper lumbar, where is it it is generally associated with cord tethering , making it more symptomatic. The two hemicords may not be equal in size , usually reunite below the level of diastematomyelia.

Type i

Type ii

There are two types:
Type I : hemicord enclosed in two separate dural sheaths with a bony,  cartilaginous or fibrous spur in between.

Type II : hemicord enclosed in same dural covering, no spur. 

In 85%  associated spinal anomalies include tethering, myelocele/myelomeningocele, lipoma, dermal sinus, dermoid or epidermoid, or meningocele.

Fenestrated Basilar MR Angiogram of Brain

Embryology of basilar :
Fusion of embryonic longitudinal neural arteries into a single basilar artery occurs in craniocaudal direction by approximately fifth fetal week. Fenestrations or "windows" within the basilar artery occur as a result of failure of fusion of the neural arteries. In severe for complete non fusion leads to duplication, this is extremely rare.


Duplication and fenestration of basilar is considered as a rare developmental anomalies.
In many case reports, the terms fenestration and duplication have been used incorrectly and interchangeably. Duplication should be strictly applied to an artery that has 2 origins and a variable course with fusion. In contrast, fenestration represents a vessel with a single origin, anywhere along its course the main trunk divides into 2 parallel segments that unite again.

Intramedullary Arachnoid Cyst of Spinal cord

Spinal Arachnoid Cysts are uncommon lesion, divided into intra dural or extra dural.
Intra dural cysts being much less common. Symptomatic spinal Arachnoid Cysts in the pediatric age group are rare.

I am posting an unusual case of intra medullary cyst of Spinal cord in a 19-year-old female who presented with lower dorsal and lumbar region pain and mild quadriparesis.

MRI study shows a solitary intra dural, unilocular, clear, Csf signal intensity cyst on ventral aspect of cord invaginating the cord best depicted on axial sections with focal expansion of cord.
Lesion is non enhancing on post contrast. No any adjacent enhancing nodule or odema.

Imaging wise possibility of an Intramedullary Arachnoid Cyst was given.
Aspiration of cyst attempted but showed recurrence which was expected.
Laminectomy with excision of the cyst done.

Intra operative and histopathological findings were suggestive of an Arachnoid Cyst.

Isolated cortical vein thrombosis MRI Brain

A 50 yo male with mild vertex headache. 

Here is his MRI Brain Axial FLAIR, T2 *GRE and non contrast 2 D TOF MR Venogram of Brain. 

This MRI study of Brain shows:
A focal vasogenic oedema in right parietal sub cortical white matter on FLAIR.
T2*GRE images show serpigenous thin cord like low signal intensities in right para sagittal parietal cortical sulci seems to be the thrombosed cortical veins. Adjacent superior sagittal sinus show normal flow voids and flow related signals on MR Venogram being not thrombosed yet. A focal flow loss of superior sagittal sinus near torcula  is artifactual due to inflow imaging.

Impression: Isolated cortical vein thrombosis. 


Terms cortical vein thrombosis and dural sinus venous thrombosis are used alternately and most of the time collectively called CVT.
They are different terms, though both are related to each and may be present simultaneously. But there can be isolated cortical vein thrombosis. Dural venous sinuse may be normal, particularly the superior sagittal sinus not yet thrombosed as in this case.

Pt was put on anticaugulants.

This is his follow up study.

The low signal intensity of thrombosed cortical veins on T2*GRE images , right parietal focal vasogenic odema has completely regressed.

Unusual sigmoid sinus lesion

A 10 yo male with right retro mastoid pain.  

Here are his MRI Brain images with non contrast 3 D TOF MR Angiogram, non contrast 2 D TOF  MR Venogram as well as axial CT sections with bone window images. 

Findings:
A well demarcated round to ovoid lesion in right sigmoid sulcus in the region of sigmoid sinus.
On MRI, a thin low signal intensity rim at the periphery on all pulse sequences, faintly getting hyperintense at the center on T2 and FLAIR images. Signals are low on T2*GRE. Lesion show intense homogeneous enhancement on post contrast T1.
Mild indentation over adjacent right cerebellum. No parenchymal invasion or perilesional odema.
No flow related signals in the region of right lateral sinus on MR Venogram.
MR Angiogram normal.
On CT, lesion is uniformly isodense with a thin hyperdense rim of uniform thickness at periphery. Bone window show no abnormal bone destruction or scalloping of adjacent bony sigmoid sulcus. Right mastoid air cells show normal pneumatisation.

Imaging wise i feel its a sigmoid sinus varix with thrombus in it.

Explanation:
Lesion is seen in sigmod sulcus in the region of sinus, no separate sigmoid sinus seen adjacent to this lesion, in consecutive sections lesion appears to be in continuity with transverse sinus so it seems to be the lesion related to sigmoid sinus itself. On CT uniform thickness hyperdense rim seem to be the normal dural outline around the abnormal focal aneurismal dilatation of right sigmoid sinus. Thrombus / blood clot in this aneurysmally dilated portion of sinus show low signal intensity on T2 and FLAIR with isointense signal on T1, lesion is isodense on CT. Enhancing thrombus on post contrast T1w images. Right lateral sinus non visualised on MR Venogram being thrombosed.