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CVD 1
CVD 1
AR DISEASE
PGI BESAS, MA. CARMINA A.
CEREBROVASCULAR DISEASE
I. Ischemic infarctions
II. Hemorrhagic
infarctions
STROKE
● Any abrupt nontraumatic
brain insult — “a blow from
an unseen hand.”
● Infarction - 75%
● Hemorrhage - 25%
● 1/3 - Emboli
○ Heart, aortic arch,
carotid arteries, or
vertebral arteries
Pathophysiologic Basis for Imaging Changes
● 20% of total cardiac output goes to the brain
○ No long term energy stores > disruption of blood
flow even for few minutes > Neuronal death
● Normal: 55 ml/100gm/min
● Minor reduction in perfusion: initially compensated
● Critical flow threshold: 10 to 20 ml/100gm/min
Imaging Findings: Acute Ischemia
● CT Scan
○ “Hyperdense Artery Sign”
○ Hyperacute sign
○ Presence of thrombus in
larger intracranial
arteries
Imaging Findings: Acute Ischemia
● Insular ribbon sign
○ Blurring of the gray-
white layers of insula
○ Early edema
○ Within 6 hours of middle
cerebral artery
occlusion
Image Findings: Acute Ischemia
● Lentiform nucleus edema
sign
○ indicates proximal MCA
occlusion.
○ can be seen as early as
one hour post onset of
stroke.
Imaging Findings: Acute Ischemia
● Diffusion-Weighted MR
○ Most sensitive for
detection of ischemia
○ “Light bulb sign”
○ Used to distinguish:
■ New ischemic areas
(high signal on DWI)
■ Older lesion: normal or
low signal on DWI
Imaging Findings: Subacute Phase
● Fogging Effect
○ Seen on 2™ week after infarction as edema and mass
effect subside
○ May present as normal sometimes
Imaging Findings: Chronic Phase
● Weeks and months following infarction
○ Macrophages remove dead tissue leaving
gliotic scar and encephalomalacia
○ CSF takes up the space previously occupied
by brain
○ Wallerian degeneration
○ Widening of adjacent sulci and “ex-vacuo”
dilatation of the ventricle
ACUTE 24 HOURS- ● Hyperdense Artery Sign
FEW DAYS ● Insular Ribbon Sign
● Lentiform Nucleus
Edema Sign
● Light Bulb Sign
SUBACUTE 2-3 WEEKS ● Fogging Event
CHRONIC MONTHS TO ● Encephalomalacia
YEARS ● Gliotic Scar
USE OF CONTRAST IN STROKE
NONCONTRAST CT CONTRAST-ENHANCED CT
● Has low toxicity, needs
● Remains the initial renal screening
radio exam of choice ● “Last” in stroke
for suspected acute protocol
stroke function ● Better in detection of
● Use to rule out non-stroke lesions
hemorrhage ● Tumor, abscess,
hematoma
Patterns of Ischemic Strokes
Watershed (Borderzone)
Infarction
● Episode of transient
global hypoperfusion
● Triggering events
○ Cardiac arrest
○ Massive bleeding
○ Anaphylaxis
○ Surgery under GA
Watershed (Borderzone) Infarction
● Rosary bead sign
○ String of small deep white
matter lesions or damage
extending out from the
corners of the lateral
ventricles on higher
sections
Small Vessel Ischemia
● Lacunes
○ Small cortical
infarcts
○ 15% to 20% of all
strokes
○ 2 to 5 mm3 cavities
○ “Little flakes”
Internal Capsule Lacunes
● Quite common and cause characteristic
syndromes.
● Receives supply from multiple perforating
arteries; ACA and MCA lenticulostriates, the ICA
anterior choroidal branch, and PCA
thalamogeniculates
Venous Infarction
● Uncommon
● Outflow blockage
● Predisposing factors
○ Hypercoagulable states
○ Pregnancy
○ Infection
○ Dehydration
○ Meningitis
Venous Infarction
● Empty Delta Sign
○ venous clot seen
indirectly as a filling
defect in the
superior sagittal
sinus on contrast-
enhanced CT
○ present 1–4 weeks
after sinus
occlusion
WATERSHED ● “corners” of the lateral
INFARCTION ventricles
● ROSARY BEAD SIGN
LACUNES ● Subcortical Infarcts
● “Little flakes”
VENOUS ● Superior sagittal sinus
INFARCT ● EMPTY DELTA SIGN
Hemorrhage
Hemorrhagic Stroke
● 10% to 20% of strokes annually
● Incidence high in:
○ Low and middle-income countries
○ Asian and African
○ Men > Women
○ Increasing age
● Noncontrast CT - modality of choice
● MR
Subarachnoid Hemorrhage
● Most common due to
aneurysm rupture
● Most common symptom:
● “Worst headache of life”
● Unruptured aneurysms may
also develop significant mass
effect with or without
headache.
● Prompt scanning is important
Subarachnoid Hemorrhage
● Most sensitive places to look
for SAH on CT:
○ interpeduncular fossa,
○ posterior sylvian fissure,
and the
○ far posterior aspects of
the occipital horns
Parenchymal Hemorrhage
Telangiectasias
● dilated capillary-sized vessels
● usually diagnosed at autopsy
● small, solitary lesions found incidentally by MR
Venous malformations
● congenitally anomalous
veins that drain normal brain
● seen in 1% to 2% of patients
studied by contrast MR
● classic appearance:
enlarged enhancing stellate
venous complex extending
to the ventricular or cortical
surface.
Other Causes of Parenchymal Hemorrhage
● Drug-Associated Hemorrhage
○ Drugs such as amphetamines and cocaine have been
commonly associated with intracranial hemorrhage.
● Amyloid angiopathy
○ increasingly recognized cause of intracranial
hemorrhage, frequently lobar in nature
○ characterized by amyloid deposits in the media and
adventitia of medium size and small cortical
leptomeningeal arteries
○ affects elderly individuals, associated with progressive
senile dementia in about 30% of cases
Epidural Hematoma
● More commonly arterial in
origin - MMA
● Lenticular or biconvex
extraaxial collections
● Temporal or Temporoparietal,
Frontal or Occipital
● Usually does not cross
cranial sutures
● Unilateral and supratentorial
Subdural Hematoma
● Venous in origin
● Mostly supratentorial and
bilateral
● Frontoparietal region
● On CT, crescent shaped
extra-axial collection of high
attenuation
● Can cross sutural margins
EPIDURAL SUBDURAL
SOURCES:
● Fundamentals of Diagnostic Radiology 4th edition, William Brant and Clyde Helms
● Harrison’s Principle of Internal Medicine 20th edition, Jameson et al
● Radiopedia, Radiolgy Masterclass