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MRI FINDINGS IN
ISCHEMIC STROKE
MODERATOR – DR.VIDHYARANI R
PRESENTER – DR. YUSRA

INTRODUCTION
• Stroke - a generic term meaning sudden onset of a neurologic
event and is also referred to as a cerebrovascular accident
(CVA).

CAUSES
• ASCO phenotypic system - which divides strokes into four subtypes:
Atherosclerotic
Small vessel disease
Cardioembolic
Others
• Hemorrhagic
Spontaneous intracranial hemorrhage
Non traumatic SAH
Venous occlusions

HYPERACUTE STAGE : < 6 HOURS
• ADC maps may depict darkening within minutes of stroke onset and
are more sensitive than diffusion-weighted sequences that are
performed after a stroke, which demonstrate hyperintensity.

MRI IN STROKE RADIOLOGY PRESENTATION...

ACUTE STAGE: 12–24 Hours
• There are further increases in the cytotoxic edema and intracellular
Ca2+.
• Activation of a wide range of enzyme systems and production of
oxygen-free radicals lead to damage of cell membranes, DNA, and
structural neuronal proteins ultimately leading to cell death.

• Cerebral edema results in prolongation of T1 and T2 relaxation
times on MRI. T2 changes (seen after 6–8 hours) are more
sensitive than T1.
• By 24 hours, 90% of patients show changes on T2-WI and only
50% show changes on T1-WI.
• Cerebral edema results in effacement of convexity sulci and mild
swelling of the gyri without mass effect.

• There may be associated subcortical hypointensity on T2 WI, which
is due to free radicals sludging of deoxygenated RBC. In addition,
thrombus may be seen as hyperintensity within the vessel lumen
(loss of normal signal void).

SUBACUTE STAGE: 2 DAYS–2 WEEKS
• There is breakdown in the BBB and rupture of swollen cells -
vasogenic edema.
• This takes about 18–24 hours to develop and becomes maximum by
48–72 hours.
• In this phase, imaging shows increased edema, mass effect, and
possible herniation depending on the size and site of the infarct.

• Signal intensity in the infarcted area remains increased on DWI
for almost 1 week and decreases thereafter, whereas reduced
ADC values peak around 3–5 days, increase thereafter, and
return to normal by 1–4 weeks.
• Gyral and parenchymal enhancement may be seen on contrast-
enhanced T1-weighted imaging and is maximal at the end of the
first week.

CHRONIC STAGE: 2 WEEKS–2 MONTHS
• The chronic stage begins with restoration of the BBB, resolution of
vasogenic edema, and cleaning up of necrotic tissue.
• This phase is characterized by local brain atrophy, gliosis, cavity
formation, and ex vacuo dilatation of the adjacent ventricle.
• Calcification and deposition of blood products (hemosiderin) may be
seen on T2 and GRE sequences.

• The incidence of hemorrhagic transformation varies greatly between
10% and 43%.
• There is alteration in the integrins and disruption of basal lamina,
collagen IV, and laminin by free radicals.
• Exposure of this disrupted endothelium to the normal vascular
pressure after clot lysis leads to reperfusion injury and extravasation
of blood. This theory is called the “reperfusion theory.”
• Susceptibility-weighted imaging such as gradient-recalled echo
(GRE) imaging, is very sensitive in the diagnosis of early
hemorrhagic transformation.

• Cortical laminar necrosis represents neuronal ischemia accompanied
by gliosis and layered deposition of fat-laden macrophages.
• On MRI, T1-WI and FLAIR sequences show hyperintensity of the
cortex that is visible 2 weeks after infarction and is most prominent at
1–3 months.
• Cystic encephalomalacia with CSF-equivalent signal intensity on all
sequences.
• Marginal gliosis or spongiosis around the old cavitated stroke is
hyperintense on FLAIR. DWI shows increased diffusivity
(hyperintense on ADC).

GRADIENT-ECHO AND SUSCEPTIBILITY-WEIGHTED
IMAGING
• Hemorrhagic Transformation - Gradient-echo and susceptibility-
weighted sequences are the most sensitive sequences.
• It is a spectrum of findings ranging from small petechial areas of
microbleeding to large parenchymal hematoma.
• These areas of bleeding are thought to be secondary to diapedesis
of red blood cells across a leaky and damaged blood-brain barrier.
This theory is called the “reperfusion theory.”

• Cortical and Pseudolaminar Necrosis - cause serpiginous cortical
T1 shortening, which is not caused by calcium or hemoglobin
products; rather, it presumably results from some other unknown
substance or paramagnetic material, possibly lipid-laden
macrophages.
• High cortical signal intensity may be seen on T1-WI, 3–5 days after
stroke and in many cases it is seen about 2 weeks after stroke.
• It increases in intensity and fades after about 3 months but in some
cases, it may persist for more than a year.

• The pattern of contrast enhancement may help determine the age of
the stroke.
• In ischemic stroke, enhancement may be arterial, meningeal, or
parenchymal.
• Arterial enhancement, the “intravascular enhancement” sign, usually
occurs first and may be seen as early as 0–2 hours after onset of
stroke.
POST CONTRAST

• It fades about 1 week after stroke, around that time parenchymal
enhancement begins and after complete infarction.
• Arterial enhancement occurs in about 50% of patients with
ischemic stroke and is most commonly seen 3 days after onset of
symptoms.
• Meningeal enhancement is the rarest type of enhancement. It
occurs within the first week after onset of stroke, usually 2–6 days,
with a peak on days 1–3.
• It usually occurs only after a large infarct in the adjacent meninges
and is thought to be secondary to reactive hyperemia.

• Parenchymal enhancement may be further subdivided into early
and late enhancement.
• It commonly begins 5–7 days after complete infarction, around the
time arterial and meningeal enhancement fades.
• In most infarcts, parenchymal enhancement is seen between 1
week and 2 months after stroke.

• If parenchymal enhancement persists longer than 8–12 weeks, a
diagnosis other than ischemic stroke should be sought.
• In cortical infarction, parenchymal enhancement may be gyriform,
and in the basal ganglia and brainstem it may be generalized or
ringlike.
• Lacunar infarcts were found to enhance more intensely than cortical
infarcts, and watershed infarcts may enhance earlier than
thromboembolic infarcts.

PENUMBRA
• Acute cerebral ischemia may result in a central irreversibly infarcted
tissue core surrounded by a peripheral region of stunned cells that is
called a penumbra.
• Brain tissue is exquisitely sensitive to ischemia, because of the
absence of neuronal energy stores.

PERFUSION MRI
• Restriction on DWI generally reflects the densely ischemic core of
the infarct while PMR depicts the surrounding “at risk” - penumbra.
• A DWI-PWI mismatch is one of the criteria for determining suitability
for intraarterial thrombolysis.

WATERSHED ("BORDER ZONE") INFARCTS
• Internal WS Infarcts - Internal "border zone" infarcts can be confluent
or partial.
• Confluent infarcts are large, cigar-shaped lesions that lie alongside
or just above the lateral ventricles.
• Partial infarcts are more discrete, rosary-like lesions. They resemble
a line of beads extending from front to back in the deep white matter.

• Stenosis or occlusion of the ipsilateral internal carotid artery or
MCA is common with unilateral lesions.
• The presence and degree of hemodynamic impairment can be
determined using a number of methods, including pCT, pMR,
SPECT, and PET.
• External (Cortical) WS Infarcts - Cortical (external) WS infarcts
are wedge or gyriform shaped.

CURRENT THROMBOLYTIC AND
NEUROINTERVENTIONAL TECHNIQUES
• Catheter-directed Intraarterial Thrombolysis
• Embolectomy and Mechanical Disruption Devices
• Intracranial Angioplasty and Stenting

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