View
15.196
Download
36
Embed Size (px)
DESCRIPTION
Citation preview
CT BRAIN - BASICSD.SUBBURAJ
PROF.G .ELANGOVAN’S UNIT
CT Principle
RING OF XRAY DETECTORS
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 --- 1000fat ---70Pure water 0Csf +8White matter +30Gray matter +45blood +70Bone/cacification +1000
CT /MRI
• CT PICTUREI. WHITE MATTER IS
DARKER THAN GREY MATTER SINCE LIPID CONTAINING MATERIAL IS RADIOLUCENT
I. 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/ cisterns2. Cortex3. Deep gray matter4. Focal lesions5. Bone6. Extracranial soft tissue7. 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
PONS4V
TEM HORN
Optic nerve
LEVEL ABOVE FOURTH VENTRICLE
SUPRA SELLAR CISTERN
MBAMB CIST
SYLV FISSURE
4V
OLF SULCUS
vermis
THIRD VENTRICULAR LEVEL
LOW VENTRICULAR
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’
M C A DOT SIGN
ATTENUATION OF LENTICULAR NUCLEUS
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
Thank u