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CT INTERPRETATION COURSE Introductory Lecture on Basic Principles ASTRACAT 2012 Part One ©iwt

CT INTERPRETATION COURSE - Cardiac and Stroke Networks in ... · In complete absence of blood flow, available energy can sustain neuronal viability for 2-3 minutes In acute stroke,

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Page 1: CT INTERPRETATION COURSE - Cardiac and Stroke Networks in ... · In complete absence of blood flow, available energy can sustain neuronal viability for 2-3 minutes In acute stroke,

CT INTERPRETATION COURSE

Introductory Lecture on Basic Principles ASTRACAT

2012

Part One

©iwt

Page 2: CT INTERPRETATION COURSE - Cardiac and Stroke Networks in ... · In complete absence of blood flow, available energy can sustain neuronal viability for 2-3 minutes In acute stroke,

“Stroke” is a Clinical Diagnosis

A clinical syndrome characterised by rapidly developing clinical symptoms

and/or signs of focal loss of cerebral function lasting more than 24 hours.

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DEFINITIONS — Stroke is classified into two major types

• Brain Ischaemia - due to thrombosis, embolism, or systemic

hypoperfusion

• Brain Haemorrhage - due to intracerebral haemorrhage or

subarachnoid haemorrhage

– A stroke is the acute neurologic injury that occurs as a result

of one of these pathologic processes

– Approximately 80 percent of strokes are due to ischaemic

cerebral infarction and 20 percent to brain haemorrhage

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Pathophysiology of stroke • An infarcted brain is pale initially.

• Within hours to days, the gray matter becomes congested with engorged,

dilated blood vessels and minute petechial hemorrhages.

• When an embolus blocking a major vessel migrates, lyses, or disperses within

minutes to days, recirculation into the infarcted area can cause a

haemorrhagic infarction

• A primary intracerebral haemorrhage damages the brain directly at the site of

the haemorrhage and by compressing the surrounding tissue

• Thrombosis generally refers to local in situ obstruction of an artery

• Embolism refers to particles of debris originating elsewhere that block arterial

access to a particular brain region

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Page 5: CT INTERPRETATION COURSE - Cardiac and Stroke Networks in ... · In complete absence of blood flow, available energy can sustain neuronal viability for 2-3 minutes In acute stroke,

What’s the point of imaging?

•Exclude haemorrhage •Determine the mechanism/cause •Differentiate infarcted tissue from salvageable tissue •Identify intravascular thrombi •Patient selection for therapy •Assess risk of complications

• Haemorrhagic transformation • Hydrocephalus in posterior circulation infarction

•Assist with prognosis

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Page 6: CT INTERPRETATION COURSE - Cardiac and Stroke Networks in ... · In complete absence of blood flow, available energy can sustain neuronal viability for 2-3 minutes In acute stroke,

CT is the best test in the acute/subacute phase

•It confidently detects or excludes haemorrhage

•Confirms the diagnosis in most cases

•Quick & patient friendly

•Easy to interpret

•Readily available

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How to Recognise Haemorrhage on CT

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Dense white “blob”

Only seen after blood clots

Minimal oedema

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“Complex” haematoma

White “blob” not homogeneous

Thalamic haematoma

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“Complex” haematoma

“Blob” not homogeneous

More white matter oedema

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Venous haemorrhage – SSS thrombosis

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Unclotted blood same density as brain – clotted blood white

NB Normal white

Matter in a young person

NOT oedema

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Acute on chronic SDH

Old

Newly clotted blood

Old & New

Mixed

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Blood clot/fluid level — anticoagulants (“complex” haematoma)

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Beware the Resolving Haematoma

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Acute

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Fading, subacute ICH

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CE CT on FU

Without previous CT, could be taken for SOL

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Final FU – atrophy at haematoma site

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Post contrast medium CT— looks like SOL

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Non contrast CT – 2 weeks earlier

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Haematoma

(Infarct) ischaemic oedema

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Normal Anatomy

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Optic tract

Substantia nigra

Red nucleus

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Insular Ribbon

CN

LN

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Th

Th = Thalamus

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Insular Ribbon Int. Caps.

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Rostrum, corpus callosum

Splenium, corpus callosum

Insular

Ribbon

ic

ic

ic

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Head of

caudate

Lentiform

Internal

Capsule

Optic radiation

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Insular ribbon

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How to Recognise an Infarct

Actually — Ischaemic Oedema

Dead infarct (core) indistinguishable from salvageable ischaemic oedema

surrounding it (penumbra)

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•Low density

•Wedge shaped

•Grey & white matter

•Within known arterial

vascular territory

•Proportionally little mass

effect

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NB Grey matter not confined

to the cortex

CN

Ant. LN

Int. caps obliterated

Subcortical infarct

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Same rules apply to MRI

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Stroke oedema?

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Stroke oedema?

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Stroke oedema?

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Stroke oedema? This small

haematoma

caused the

“stroke”

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Stroke oedema? Complex SOL

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Stroke? — MRI — Same rules

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Hyperdense MCA

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Dense ICA

Plus fleck of

Calcification in

Vessel wall

Dense MCA

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Hyperdense MCA with Fragmentation

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More Subtle Examples of Early Infarction

Basic neuroanatomy to support early

diagnosis

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Insular Ribbon

CN

LN

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Insular Ribbon Int. Caps.

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Rostrum, corpus callosum

Splenium, corpus callosum

Insular

Ribbon

ic

ic

ic

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Page 56: CT INTERPRETATION COURSE - Cardiac and Stroke Networks in ... · In complete absence of blood flow, available energy can sustain neuronal viability for 2-3 minutes In acute stroke,

Head of caudate

Lentiform

Internal

Capsule

Optic radiation

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Insular ribbon

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Insular Ribbon & BG signs

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Early Infarction & FU

(Insular ribbon & BG signs)

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Insular Ribbon, BG & CN– obliterated on Right. Normal on Left. Blue stars = Insula. Yellow star = BG

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CN

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Reduced attenuation (low density)

obliterates grey/white differentiation

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Next day

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Insular Ribbon Int. Caps.

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Rostrum, corpus callosum

Splenium, corpus callosum

Insular

Ribbon

ic

ic

ic

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Ext caps

CN

LN

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Day 1

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Day 2

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Day 4

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Haemorrhagic Infarction

and how to tell it from a primary

intracerebral haemorrhage

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New

H’gic

infarct

Old

Infarct

Why?

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Pt with SBE throwing off multiple emboli

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Plain CT – haemorrhagic infarction

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ICH

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Contrast Enhancement in Infarction

Luxury perfusion and the blood brain

barrier

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Plain CT

CE CT

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NC CE

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NC CE

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CE CE

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“Special” Infarcts

or unusual consequences

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BG (Pallidal) Infarction – CO Poisoning

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Bilateral BG/Ext Caps Infarction

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Post Cardiac Arrest Infarction Cortical Mantle

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Post Arrest Plain CT

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Post CE — Acute Cortical Laminar Necrosis

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Acute Occlusion ICA > ACA/MCA Infarction > Malignant Oedema >

Herniation > Venous Congestion & Haemorrhage

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Raised ICP with h’age often mistaken for SAH

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Normal CT

Then Effect of Sudden Rise in ICP

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Intradural venous congestion over tent looks like SAH

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“Watershed” Infarcts ie Border Zone

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©Radiology Assistant

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How to Recognise the Different Vascular Territories

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lat midline

from top from below

Red = MCA

Green = ACA

Purple = PCA

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Circle of Willis rarely

a true circle

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No circle at all

No Post.Comm. Arteries

Ant & Post circulation isolated

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Dominant Post Comm

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ICA occlusion – ACA & MCA infarcts

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MCA & PCA infarcts because of dominant

Post Comm Art on Right

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Carotid Artery Dissection

No infarct

Circle of Willis protects brain

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Polo Mint – thrombus in arterial wall, end on Thrombus en face

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C of W protects

No infarct

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C of W protects via Ant Comm

No infarct

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Vascular Territories (contd) - PCA

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PCA

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How to Select Patients for thrombolysis?

• Clinical — NIHSS

• Infarct size — ASPECT Score

• Distinguishing dead tissue from living, but stunned, brain —

CT Perfusion

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How to Select Patients for thrombolysis?

• Clinical — NIHSS

• Infarct size — ASPECT Score

• Distinguishing dead tissue from living, but stunned, brain —

CT Perfusion

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ASPECT Scoring System

•A = ACA; P = PCA; M = MCA

•MCA territory (10 points is Normal)

• Subtract one point for each:

• M1, M2, M3

• M4, M5, M6

• Caudate, Int Caps, LN, Insula

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c LN

ic In

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Level with foramina of Monro

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M1

M2

M3

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Sylvian fissure

Level with 3rd V

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M4

M5

M6

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(VRS)

Level with top of Lat Vs

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ASPECTS

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Examples from paper

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How to Select Patients for thrombolysis?

• Clinical — NIHSS

• Infarct size — ASPECT Score

• Distinguishing dead tissue from living, but stunned, brain —

CT Perfusion

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Penumbra

Unlike muscle, brain tissue exquisitely sensitive to ischaemia

Absence of neuronal energy stores

In complete absence of blood flow, available energy can sustain neuronal

viability for 2-3 minutes

In acute stroke, ischaemia incomplete

Collateral blood supply from uninjured arterial & leptomeningeal territories

Results in central infarcted tissue surrounded by peripheral

“stunned” cells (penumbra)

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Imaging of the Penumbra

CT

Discrepancy in perfusion parameters

MRI

Mismatch between diffusion & perfusion parameters

(DWI/PWI)

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CT Perfusion Imaging

CBF = CBV/MTT

CBV = area under parenchymal curve/area under arterial

curve

MTT calculated from time difference between arterial inflow

& venous outflow + time to peak enhancement

Penumbra -v-Dead tissue

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Pericallosal artery Sigmoid (venous) sinus

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CBV CBF MTT

CTP

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Normal CT

CTP – perfusion defect

CTA – ICA dissection

© radiology assistant

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CTA

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Normal CTA

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Hypodensity Right Insula — CTA

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Taken from “Radiographics, October 2006”

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Goals of Acute Stroke Imaging The Four Ps

Parenchyma Assess early signs of acute stroke Rule out haemorrhage

Pipes – look for intravascular thrombus Extracranial circulation (neck) Intracranial circulation

Perfusion Cerebral blood volume Cerebral blood flow Mean transit time

Penumbra Tissue at risk

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Conclusions

Stroke is a clinical diagnosis

CT is best and will suffice in majority

MR for CT neg. stroke or

for definitive diagnosis when suggested clinically eg

dissection or

where CT suggests alternative diagnosis eg SOL

Advanced MR techniques best left to specialist units

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DDX of Arterial Infarction

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Not all Infarction is Arterial

Venous Infarction

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Venous sinus thrombosis

•Low incidence [<1 in 10,000 persons]

•Risks factors

• Tissue damage and stasis

• Haematological disorders

• Malignancies

• Collagen vascular disorders

• Pregnancy

• Medications

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Venous sinus thrombosis

•CT brain shows non-arterial distribution infarcts in the white matter and/or cortical white matter junction, often associated with haemorrhage

•Empty delta sign on contrast-enhanced CT scan

•Occasionally, the cortical veins can be seen with fresh thrombus within.

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MR and MR Venography

•Advantages • sensitive to blood and

parenchymal changes • Cortical vein thrombosis and

sinus thrombosis can be identified with multiple appropriate sequences

•Disadvantages • Difficult to recognise thrombus

in first few days on conventional MRI

• Flow and susceptibility artefacts and saturation effects in TOF can make interpretation difficult

• Difficult in unwell patients • Contraindications to MRI • Expensive and availability

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CT Venogram

• Advantages

• Can be added as an adjunct to unenhanced CT - Non invasive

• Not expensive, reliable and easy to interpret

• Fast acquisition reduces motion artefacts

• Monitoring of critically ill patients is easier.

• Can differentiate slow flow from thrombus, which is a problem with MRI.

• Disadvantages

• Radiation (Mean effective dose <2.2 mSV)

• Contrast media flow dynamics not seen as well as in DSA

• Metallic artefacts may impair visualisation of venous structures

• Contraindicated in pregnancy

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Normal CTV Anatomy

For interest only

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Normal radiological cerebral venous anatomy

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Normal radiological cerebral venous anatomy

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Deep veins

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Outflow tracts

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Normal Variants

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Asymmetric transverse sinus

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Venous thrombosis

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Empty Delta Sign (SSS = sup sag sinus & TS = transverse sinus)

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Venous sinus thrombosis

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Arrows point to Empty Delta Sign

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Example:

Plain T1W MRI

Bilat. Parasagittal H’age

Thrombus in SSS

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MRV showing non-filling of SSS and SS