CT BRAIN - BASICS

D.SUBBURAJ

PROF.G .ELANGOVAN’S UNIT

CT Principle

FOURTH GENERATION

RING OF XRAY DETECTORS

X ray gun

Frankfurt plane

HOUNSFIELD UNITS

• Numeric information in each pixel of ct image

• Related to composition & nature of tissue

• Represent the density of tissue

• Also called as CT NUMBER

air --- 1000

fat ---70

Pure water 0

Csf +8

White matter +30

Gray matter +45

blood +70

Bone/calcification +1000

CT /MRI

• CT PICTURE• WHITE MATTER IS

DARKER THAN GREY MATTER SINCE LIPID CONTAINING MATERIAL IS RADIOLUCENT

IV. CSF IS BLACK

• MR PICTURE GREY GREY

MATTERMATTERT1WIDARK

T2WI

BRIGHT

WHITE WHITE MATTRMATTR

BRIGHT DARK

CSFCSF 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

TEMBORAL HORN

OCCIPITAL HORN

FORAMEN OF MONRO

4 V

AQUEDUCT OF SYLVIUS

3V

trigone

COMMON SECTIONSAXIAL SECTIONS CORONAL SECTIONS SAGITTAL SECTIONS

POSTERIOR FOSSA CUTS-ABOVE THE FORAMEN MAGNUM LEVEL

-LEVEL OF THE FOURTH VENTRICLE

-ABOVE THE FOURTH VENTRICULAR LEVEL

- TENTORIAL

SUPRATENTORIAL CUTS

-THIRD VENTRICULAR LEVEL

-LOW VENTRICULAR LEVEL

-ABOVE THE VENTRICULAR LEVEL

-FRONTAL HORN LEVEL

-THIRD VENTRICULAR LEVEL

-MID VENTRICULAR LEVEL

-OCCIPITAL HORN LEVEL

-MID SAGITTAL LEVEL

-PARASAGITTAL LEVEL THROUGH THE LATERAL VENTRICULAR BODY

-LATERAL ORBITAL LEVEL

ABOVE THE LEVEL OF FORAMEN MAGNUM

VAMEDULLA

TONSIL4 V

CMINT OCC PROT

LEVEL OF FOURTH VENTRICLE

MCP

CPCISTERN

PONS

4V

TEM HORN

Optic nerve

LEVEL ABOVE FOURTH VENTRICLE

SUPRA SELLAR CISTERN

MBAMB CIST

SYLV FISSURE

4V

OLF SULCUS

vermis

THIRD VENTRICULAR LEVEL

Foramen of monro

3 V

SUPRA CEREBELLAR CISTERN

VERMIS

INSULA

TRIGONE

LOW VENTRICULAR LAT VEN

3 V

HEAD OF CAUDATE

THALAMUS

LENTIFORM NUCLEUS

INSULAR RIBBON

Above ventricle level

Cerebral Arterial Territory

• MCA-most of lateral hemisphere, Basal ganglia, insula,

• ACA-Inferomedial basal ganglia,ventromedial frontal lobes, anterior 2/3rd medial cerebral hemispheres, 1 cm supero medial brain convexity

• PCA-Thalami, midbrain, posterior 1/3of medial hemisphere, occipital lobe, postero medial temporal lobe

• Anterior Choroidal arterybranch of ICA supply part of the hippocampus, the posterior limb of the internal capsule

• Medial lenticulostriate arteriesBranches 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 arteriesBranches 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

MCAACA

PCA

• AICA- inferolateral part of pons, middle cerebellar peduncle, floccular region, anterior petrosal surface of cerebellar hemisphere

• PICA-posteroinferior surface of cerebellar hemisphere , ipsilateral part of inferior vermis,

• Superior cerebellar artery-superior aspect of cerebellar hemisphere (tentorial surface), ipsilateral superior vermis, largest part of deep white matter including dentate nucleus, pons

Water shed infarct

CEREBRAL ISCHEMIA

Cerebral ischemia

• Significantly diminished blood supply to all parts(global ischemia) or selected areas(regional or focal ischemia) of the brain

• 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 severity In the central core of the infarct, the severity of hypoperfusion results in irreversible of hypoperfusion results in irreversible cellular damage . cellular damage .

• Around this core, there is a region of decreased flow Around this core, there is a region of decreased flow in which either:in which either:– The critical flow threshold for cell death The critical flow threshold for cell death

has not reached has not reached – Or the duration of ischemia has been Or 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 - 48 hours)Acute infarct(12 - 48 hours)

• Subacute infarct(2 - 14 days)Subacute infarct(2 - 14 days)

• Chronic infarct(>2 weeks)Chronic infarct(>2 weeks)

• Old infarct(>2 monthsOld 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 loss along the lateral insula

Dense mca sign

‘ loss of insular ribbon’ LeftLeft

M C A DOT SIGN

ATTENUATION OF LENTICULAR NUCLEUS Left side

CT- Acute infarct

• Low density basal ganglia

• Sulcal effacement

• Wedge shaphed parenchymal hypo density area that involves both grey and white 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 weeks, disappears by 2 months

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

• CECT: No enhancement

INFARCT / TUMOUR

• CLINICAL HISTROY

• DISTRIBUTION

• SHAPES

• GRAY / WHITE INVOLVEMENT

• ADVANCED IMAGING

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

• EDEMA

NOT CONFINED TO VASCULAR DISTRIBUTION

MOSTLY INVOLVES WHITE MATTER

PCA INFARCT

MCA INFARCT

ACA INFARCT

WATERSHED INFARCTWATERSHED INFARCT

Old infarct

H’gic infarct

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