CT Basics

C

Frankfurt plan

HOUNSFIELD UNITS

HOUNSFIELD UNITS

•• _{Numeric information in Numeric information in each each pixel pixel of of ctct}

image image

•• _{Related to composition & nature of tissueRelated to composition & nature of tissue} •• _{eepprreesseennt t tt e e eennss tty y o o tt ssssuuee}

a aiirr --- 11000000 f faatt ---7700 P Puurre e wwaatteerr 00 W Whhiitte e mmaatttteerr ++3300 G Grraay y mmaatttteerr ++4455 b blloooodd ++7700 B Boonnee//ccaacciiffiiccaattiioonn ++11000000

CT /MRI

• _{CT PICTURE}

I. WHITE MATTER IS DARKER THAN GREY MATTER SINCE LIPID

• _{MR PICTURE} GREY GREY MATTER MATTER T1WI DARK T2WI BRIGHT WHITE

WHITE BRIGHT DARK

CONTAINING MATERIAL IS RADIOLUCENT  I. CSF IS BLACK CSF CSF GREY TO DARK WHITE

Step wise approach

1. Ventricles/ cisterns

2. Cortex

3. Deep gray matter 4. Focal lesions

5. Bone

6. Extracranial soft tissue 7. Para nasal sinuses

LV FRONTAL HORN OCCIPITAL HORN 3V TEMBORAL HORN FORAMEN OF MONRO 4 V AQUEDUCT OF SYLVIUS

COMMON SECTIONS

AXIAL SECTIONS CORONAL SECTIONS SAGITTAL SECTIONS

POSTERIOR FOSSA CUTS

-ABOVE THE FORAMEN MAGNUM LEVEL

-LEVEL OF THE FOURTH VENTRICLE

--FRONTAL HORN LEVEL -THIRD VENTRICULAR LEVEL

-MID VENTRICULAR

-MID SAGITTAL LEVEL

-PARASAGITTAL LEVEL THROUGH THE LATERAL VENTRICULAR BODY VENTRICULAR LEVEL - TENTORIAL SUPRATENTORIAL CUTS -THIRD VENTRICULAR LEVEL

-LOW VENTRICULAR LEVEL -ABOVE THE VENTRICULAR LEVEL

LEVEL

-OCCIPITAL HORN LEVEL -LATERAL ORBITAL LEVEL

ABOVE THE LEVEL OF FORAMEN MAGNUM

VA

MEDULLA

TONSIL 4 V

CM

LEVEL OF FOURTH VENTRICLE Optic nerve MCP CPCISTERN PONS 4V TEM HORN

LEVEL ABOVE FOURTH VENTRICLE

SUPRA SELLAR CISTERN 

SYLV FISSURE OLF SULCUS MB AMB CIST 4V  vermis

Cerebral Arterial Territory

•

_MCA

_{-most of lateral hemisphere, Basal}

ganglia, insula,

•

_ACA-

_{Inferomedial basal ganglia,ventromedial}

,

hemispheres, 1 cm supero medial brain convexity

•

_PCA

_{-Thalami, midbrain, posterior 1/3of} 

medial hemisphere, occipital lobe, postero medial temporal lobe

• _{Anterior Choroidal artery} 

branch of ICA supply part of the hippocampus, the posterior limb of the internal capsule

• _{Medial lenticulostriate arteries}

Branches of the A1-segment of the anterior cerebral  artery.

They supply the anterior inferior parts of the basal nuclei and the anterior limb of the internal capsule.

• _{Lateral lenticulostriate arteries}

Branches of the horizontal M1-segment of the middle cerebral artery .

They supply the superior part of the head and the body of the caudate nucleus, lentiform nucleus and the posterior limb of the internal capsule

MCA

ACA

• _{AICA- inferolateral part of pons, middle}

cerebellar peduncle, floccular region, anterior petrosal surface of cerebellar hemisphere

• _{PICA-posteroinferior surface of cerebellar}

, ,

• _{Superior cerebellar artery -superior aspect of} 

cerebellar hemisphere (tentorial surface),

ipsilateral superior vermis, largest part of deep white matter including dentate nucleus, pons

CEREBRAL

ISCHEMIA

CEREBRAL

ISCHEMIA

Cerebral ischemia

•

_{Significantly diminished blood supply to}

all parts(global ischemia) or selected

areas(regional or focal ischemia) of the

ra n

•

_{Focal ischemia- cerebral infarction}

•

_{Global ischemia-hypoxic ischemic}

encephalopathy(HIE),hypotensive

cerebral infarction

Goal of imaging

• _{Exclude hemorrhage}

• _{Identify the presence of an underlying structural}

lesion such as tumour , vascular malformation ,subdual hematoma that can mimic stroke

• _{Identify stenosis or occlusion of major extra- and}

intracranial arteries

• _{Differentiate between irreversibly affected brain}

tissue and reversibly impaired tissue (dead tissue versus tissue at risk)

Infarct vs pneumbra

•• _{In the central core of the infarct, the severityIn the central core of the infarct, the severity}

of 

of hypoperfusionhypoperfusion results in irreversibleresults in irreversible cellular damage . cellular damage . ,, in which either: in which either:  –

 – _{The critical flow threshold for cell deathThe critical flow threshold for cell death}

has not reached has not reached

 –

 – _{Or the duration of ischemia has beenOr the duration of ischemia has been}

insufficient to cause irreversible damage. insufficient to cause irreversible damage.

••

_{Hyper acute infarct(<12 hours)}

_{Hyper acute infarct(<12 hours)}

••

_{Acute infarct(12}

_{Acute infarct(12 -- 48 hours)}

_{48 hours)}

••

_Subacute

_{Subacute infarct 2}

_{infarct 2 -- 14 da s}

_{14 da s}

••

_{Chronic infarct(>2 weeks)}

_{Chronic infarct(>2 weeks)}

••

_{Old infarct(>2 months}

_{Old infarct(>2 months}

₎

CT-Hyperacute infarct

•

_{Hyperdense MCA sign}

_{-acute intraluminal}

thrombus

• _{Attenuation of lentiform nulei}

•

_{Dot sign}

_{-occluded MCA branch in sylvian}

fissure

•

_{Insular ribbon sign}

 _{–grey white interface}

ATTENUATION OF LENTICULAR

NUCLEUS

CT- Acute infarct

• _{Low density basal ganglia} • _{Sulcal effacement}

• _{Wedge shaphed parenchymal hypo density}

area t at nvo ves ot grey an w te matter

• _{Increasing mass effect}

• _{Hemorrhagic transformation may occur -15}

to 45% ( basal ganglia and cortex common site) in 24 to 48 hours

CT – sub acute infarct

• _{PLAIN CT}

• _{Wedge-shaped area of decreased attenuation involving}

gray/white matter in typical vascular distribution

• _{Mass effect initially increases, then begins to}

diminish by 7-10 days

• _{H’gic transformation occurs in 15-20% of MCA occlusions,}

usually by 48-72 hrs

• _CECT

• _{Enhancement patterns typically patchy}

• _{May appear as early as 2-3 days , persisting up to 8-10}

weeks

• _{"2-2-2" rule = enhancement begins at 2 days, peaks at 2}

CT-chronic infarct

•

_{Plain ct}

• _{Focal, well-delineated low-attenuation areas}

in affected vascular distribution

• _{sulci become prominent; ipsilateral ventricle}

enlarges

• _{Dystrophic Ca++ may occur in infarcted brain}

but is very rare

INFARCT / TUMOUR

•

_{CLINICAL HISTROY}

•

_DISTRIBUTION

•

_SHAPES

•

_{GRAY / WHITE INVOLVEMENT}

VENOUS INFARCT

• _HISTROY

• _{BEYOND VASCULAR DISTRIBUTION} • _{HAEMORRHAGIC INFARCT}

• _{THORMBUS IN VENOUS SINUSES}

• _{SYMMETRICAL LOW ATTENUATION IN DEEP}

GRAY MATTER - DEEP CEREBRAL VEIN THORMBUS

EDEMA/ INFARCT

• _INFARCT

TYPICAL VASCULAR DISTRIBUTION GRAY MATTER INVOLVEMENT

•

NOT CONFINED TO VASCULAR DISTRIBUTION MOSTLY INVOLVES WHITE MATTER

MCA INFARCT

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WATERSHED INFARCT

WATERSHED INFARCT