2. Definition
A NEUROLOGICAL DEFICITOF
▪ Sudden onset
▪ With focal rather than global dysfunction
▪ In which, after adequate investigations,
symptoms are presumed to be of non-
traumatic vascular origin
▪ and lasts for >24 hours
3. Functional loss of cell
CYTOTOXICEDEMA,
CELL DEATH
Increased water content
VASOGENIC EDEMA
MASS EFFECT
GLIOSIS
MINUTES
12-24 hrs
24hrs-2wks
PATHOPHYSIOLOGY
Reduced blood flow
Autoregulation
4. Role of imaging in ischemic stroke
▪ To rule out mimics esp hemorrhage
▪ To suggest the therapeutic role
▪ To establish the etiology
5. Stroke – Temporal phases
▪ Early Hyperacute – 0-6hrs
▪ Late Hyperacute 6 to 24 hrs
▪ Acute- 24 hrs to one week
▪ Subacute- 1 to 3 weeks
▪ Chronic- > 3wks
6. NCCT in stroke
▪ Very sensitive in detecting hemorrhage
▪ Other mimics ruled out-
ISCHEMIA SUSPECTED
7. Early CT findings
A) Hypoattenuating grey matter structures
B)Presence of one or more hyperattenuating
arteries
C)Early Mass effect
10. NCCT in acute stroke
▪ OTHER EARLY SIGNS
Loss of grey white matter differentiation
Early mass effect-
Narrowing of sylvian fissure
Loss of cortical sulci
11. Hyperdense MCA sign
ONLY REVERSIBLE EARLYSIGN
▪ MCA occluded by fresh thrombus
▪ -specificity- 100%, sensitivity -30%
▪ Hyperdense MCA can also be seen
➢high
hematocrit level
➢calcification
in such cases –
usually bilateral
13. NCCT
▪ Importance of window settings
Normal settings- w80 HU,C- 20HU
W- 8HU- C-32 HU
SENSITIVITYINCREASED
14. NCCT
▪ Advantages
very useful to exclude hemorrhage
widely accessible
convenient
short imaging time
▪ Disadvantages
findings are subtle
not useful for ischemic penumbra
Not useful for posterior fossa infarcts
15. MRI in stroke
DWI
Most sensitive sequence in stroke imaging
High intensity in DWI indicate restriction of the
ability of water proton to diffuse extracellularly.
37. Watershed infarcts
▪ Junction of large arterial territories
▪ Chronic large vessel stenosis precipitated
by hypotension
▪ DWI , PW helpful in etiology
40. CTA
▪ Fast, thin section,volumetric spiralCT
examination performed with a time-
optimized bolus of contrast material for the
opacification of vessels.
41. CTA- Source images
▪ Occlusion ,stenosis or
significant calcification
of an Extracranial
internal carotid artery
▪ Detection of hyperacute
infarct
▪ Substraction perfusion
42.
43. CTA- adv
▪ Volume rendering.
▪ Groups of voxels within defined attenuation
thresholds are selected,and a color as well as
an “opacity” is assigned
46. MRA - techniques
▪ TOF techniques
use of gradient pulses withTRshorter than
background tissue– Flow related
enhancement of inflowing nuclei
▪ 2D technique- individual slices
useful in slow flow states
▪ 3D techniques-A volume of slab
useful in high flow states
Better spacial resolution
47. CE MRA
RAPID 3D GRADIENT ECHO (GRE) SEQUENCE FIRST PASS MRA USINGA
SELECTIVELY LARGE BOLUS OF GADOLINIUM BASEDCONTRAST.
▪
ADVANTAGES :
NOT SUSCEPTIBLETO SIGNAL LOSS FROMTURBULENCEOR SLOW FLOW
COMPAREDWITHTOF OR PCTECHNIQUE
▪ ALLOWS BETTERVESSELTO BACKGROUNDCONTRASTCOMPAREDWITH
TOF /PC
▪ SHORTER IMAGINGTIME
▪ LESS SUSCEPTIBLETO MOTIONARTIFACTS
▪ ALLOWS IDENTIFICATION OF SLOW FLOW IN NEARLYOCCLUDEDVESSEL
▪ ALLOWS MORE ACCURATEASSESSMENTOF STENOSIS &VISUALIZATION
OF ULCERATED PLAGUE
53. CT- perfusion parameters
▪
▪
▪
▪
CEREBRAL BLOODVOLUME the volume of blood
per unit of brain tissue
CEREBRAL BLOOD FLOW the volume of blood
flow per unit of brain tissue per minute
MEANTRANSITTIME, the time difference
between the arterial inflow and venous
outflow
TIMETO PEAK ENHANCEMENT the time from the
beginning of contrast material injection to
peak enhancement
54. CT perfusion - Interpretation
M TT CBF CBV
Arterial stenosis normal normal
Oligaemia
(>60%)
near normal
Penumbra
(>30%)
Normal or
increased
Infarct
(<30%) (<40%)
