NEUROIMAGING

NEUROIMAGING
of
CEREBROVASCULAR
DISEASE James G. Smirniotopoulos, M.D.
Uniformed Services University
of the Health Sciences
Bethesda, MD

**Before you begin:**
	Vascular Territory Maps
	Basic Neuroanatomy

STROKE:

A sudden loss or dimunition in neurologic function caused by the rupture or obstruction of an artery of the brain.

CEREBROVASCULAR DISEASE
(CVD):

Any abnormality of the brain resulting from a pathologic process in the cerebral circulation or vessels.

CEREBROVASCULAR DISEASE

Dilatation/Enlargement
Narrowing/Obstruction
Disruption of Vessel

CEREBROVASCULAR DISEASE

Mass Effect
Ischemia / Infarction
Hemorrhage

"STROKE"

500,000 per year in USA
200,000 deaths/year
28,000 are Aneurysm rupture

"STROKE"

2.5 Million "stroke" survivors in USA
15% Totally disabled
55% Require ongoing special care

Aneurysm and Rupture

Clinical Hx:
Worst Headache of My Life
Nuchal Rigidity (meningismus)
Photophobia
Localizing Signs

Aneurysm and Rupture

Demographics:
Common Cause of Stroke in Adults
Peak at 40-60yr
Risk Factors: Hypertension

Aneurysm and Rupture

Aneurysm Incidence:
1-8% of unselected Adult Autopsies
Implies most are ASYMPTOMATIC
Familial, ADPCKD

Subarachnoid Hemorrhage:

LP more sensitive than CT
Trauma is most common cause of SAH
CT detected SAH is usually Aneursym / AVM

Aneurysm and Rupture

SPASM - Infarction
HEMATOMA - Herniation, etc.
Re-BLEEDING
HYDROCEPHALUS

Aneurysm and Rupture

LOCATION of ANEURYSM
80-85% Anterior Circulation
15-20% Posterior/Vertebral

Aneurysm and Rupture

ANGIOGRAPHY:
Location of Aneurysm
Multiple (25% are)
Visualize "Neck"
Spasm ?
If (-) REPEAT in 2-3 wks.

"SPONTANEOUS" HEMORRHAGE
(Non-Traumatic)

SPONTANEOUS HEMORRHAGE

Berry Aneurysm
Leukemia (decreased platelets)
Neoplasms (Primary/Secondary)
Angiomas (AVM, Cavernous, Moya-Moya)
Vasculitis (SLE, etc.)
Venous/Sinus thrombosis
"Hypertensive"

Neoplastic Hemorrhage

CNS Primary Neoplasm
2/3 of neoplastic bleeds
CNS Secondary (Metastatic)
1/3 of neoplastic bleeds

Neoplastic Hemorrhage

CNS Primary Neoplasm
2/3 of neoplastic bleeds
Glioblastoma Multiforme
Oligodendroglioma
CPP, PNET, etc.

Neoplastic Hemorrhage

CNS Secondary (Metastatic)
1/3 of neoplastic bleeds
Choriocarcinoma
Melanoma
Thyroid
Breast
Renal
Lung

VASCULAR MALFORMATIONS

Vascular Malformations

Arterio-Venous-Malformation (AVM)
Cavernous Malformation (Hemangioma)
Venous Malformation (Varix)
Telangiectasia (Capillary, Venous)
Transitional (Complex) Forms

Vascular Malformations

Arterio-Venous-Malformation (AVM)
NIDUS (has shunt)
Dilated aa. and vv.
Embedded within
Parenchyma / Gliosis
Minimal mass effect (w/o bleed)
Intact BBB (no edema)
Dystrophic Ca++
Atrophy ("steal")

Vascular Malformations

Arterio-Venous-Malformation (AVM)
Hemorrhage
Mass effect
Hyperdense on NCT (acute)
Complex Signal on MRI

Vein of Galen Malformation

High Output Failure
Congestive Failure / PDA
Hydrocephalus
Obstruction at Aqueduct
CNS Venous Hypertension
Cranial Bruit

Vein of Galen Malformation

Direct Fistula
Parenchymal AVM (shunt)
Hypoplasia of Straight Sinus
Intrauterine Sinus Thrombosis

Cavernous Malformations

Hereditary (multiple)
Variable sized vascular spaces
capillaries, sinusoids, no brain
Slow Flow (delayed opacification)
Angiographically "occult"
Mass, Dystrophic Ca++, Enhancement
Blood Breakdown Products
methemoglobin (white T1W)
hemosiderin (dark T2W)

Venous Malformations (Varix)

abnormal vascular development
insufficient cortical veins
"dominant" TRANSCORTICAL VEIN
drains unusually large territory
smaller parenchymal veins converge
Flow Void/Enhancement
Tubular (transcortical vein)
Crown of radiating vv. ("Medusa")

Vascular Malformations

Arterio-Venous Malformations
White Worms on ECT
Black Worms on MRI
Enhancement and flow void

CEREBROVASCULAR DISEASE:

Cerebral Infarction

BRAIN

1/50 of body weight
1/6 of cardiac output
1/5 of Oxygen

NORMAL CEREBRAL BLOOD FLOW:

Gray matter 4x white matter
Cortex = 1.69 ml/gm/min
Callosum - 0.40 ml/gm/min

Infarction

INFARCTS with BLOOD
HEMORRHAGIC
INFARCTS w/o BLOOD
ISCHEMIC

Classification of Infarction

HISTOLOGY
MORPHOLOGY
ETIOLOGY

Classification of Infarction

HISTOLOGY
Hemorrhagic
Anemic
MORPHOLOGY
Wedge (arterial)
Border Zone (flow)
Laminar, etc.
ETIOLOGY
Arterial Thrombosis
Arterial Embolus, Herniation
Venous Thrombosis
Hypotension, Anoxia

Homeostasis

Autoregulation of Blood Flow
Circle of Willis
"Pial" Collaterals
distal anastomoses

Autoregulation

Most tissues have "pressure passive" flow
CNS locally regulates flow based on metabolism
(basis for fMRI)
pre-capillary arteriole
pCO2, pH, pO2 control it
range of mean pressure for regulation: 60 - 150 mm Hg

Ischemic Infarction

PALE, WHITE
BLAND
ANEMIC, ISCHEMIC

Ischemic Infarction

Non-Hemorrhagic
Arterial Thrombosis, Hypotension
Larger Vessel, Large Infarct
Atherosclerosis

Imaging of Infarction

EDEMA
Cytoxic (Gray and White)
Vasogenic (White only)
Enhancement
Abnormal BBB
"Luxury Perfusion"
Hyperdense / Hyperintense MCA
Vessel enhancement w/Gd

Infarct - Low Density

NO BLOOD - Anemic Cortex
EDEMA
Cytotoxic (Gray and White)
Vasogenic (White only)
ENCEPHALOMALACIA
necrosis
phagocytosis (encephaloclysis)

Ischemic Infarction

Increased Water (Edema)
Low density on CT
Bright on T2W MR
Gray and/or White Matter
SHAPE - vascular wedge
MASS EFFECT
may be minimal
cortical (effacement of sulci)
Peaks at 3-5 days

PATTERNS OF EDEMA

AJNR 3:251-255, 1982
VASOGENIC SPREAD
(neovascular edema)
4/339 (1.2%) INFARCTS
GRAY MATTER EDEMA
(cytotoxic edema)
2/155 (1.3%) TUMORS

Ischemic Infarction

Location of Infarction
MCA 62%
PCA 14%
ACA 5%
Pofo 5%
Multiple, Watershed 14%

Ischemic Infarction

Increased Water
cytotoxic edema
Prolonged T1/T2, Decreased density
Decreased Attenuation on NCT
+/- Sl. darker on T1W MRI
Sl. brighter on PD
Bright on T2W MRI

WHAT ABOUT CONTRAST?

If an infarct is caused by a loss of blood flow, then how do water and contrast get there?
Re-perfusion
collaterals (early)
recanalization (late)
healing (late)
CONTRAST TOXICITY
Osmolarity
BBB damage
Circulatory effects
Hypotension
Vaso-vagal attack

"Ischemic Enhancement"

Misnomer?
Contrast delivered by flow
Cortical Gray - "Gyriform" pattern
Etiology:
increased flow
Abnl. BBB outside infarct
Abnl. BBB during healing of infarct

"Luxury Perfusion"

Angiographic term
increased perfusion/vascularity
implies re-perfusion

"Ischemic Enhancement"

Early ("immediate") uncommon
Early (4-6 hrs.)
SUBACUTE (7-12 days)
PEAK in amount and incidence
LATE (6-9 months)
PERSISTENT (1-2 years) uncommon

"Ischemic Enhancement"

(Reperfusion in min. to hrs.)
"LUXURY PERFUSION"
BBBB (> 4 - 6 hrs. of ischemia)
original capillaries affected
New Capillaries (7-10 days) grow into infarct for healing w/o BBB

"LUXURY PERFUSION"

Angiographic observation
FOCAL HYPEREMIA (relative or absolute)
CORTICAL BLUSH and EARLY VEINS
shunting
LOSS OF AUTOREGULATION
(caused by inc. pCO2, decr. pH/pO2)
TRANSIENT
minutes to hours, ends in 3-5 days

CEREBROVASCULAR DISEASE:

Hemorrhagic Infarction

Hemorrhagic Infarction

ARTERIAL ETIOLOGY
Embolic Occlusion (MCA)
Herniation (PCA, AChA)
VENOUS ETIOLOGY
Sinus Thrombosis (SSST)
infarcts in strips, parallel falx
CONVERSION in ISCHEMIC INFARCT
Large Infarcts
Anticoagulation (incl. ASA)

Hemorrhagic Infarction

IMAGING HEMORRHAGIC INFARCTION
can be smaller in embolic (MCA)
can be larger in herniation (PCA, AChA)
Petechial Hemorrhage into Cortex
ISO- to HYPER- dense on NCT
BRIGHT on T1W MRI
Enhance Early and Intensely
NM scans positive EARLY

Hemorrhagic Infarction

HEPARIN CONTRAINDICATIONS
neoplasm
AVM, aneurysm, SAH
grossly hemorrhagic mass
LARGE infarcts, any cause
Hemorrhagic Infarction?
Embolic Etiology?

EXCEDRIN HEADACHE #27:

(4:00 AM)
"CAN I ANTICOAGULATE?"

HEPARIN:

Stroke-In-Evolution
progression of vascular territory
Embolic Stroke

HEPARIN CONTRAINDICATIONS:

Neoplasm
AVM, aneurysm
Grossly hemorrhagic
Large infarcts
Hemorrhagic infarct?
(embolic infarction)

EMBOLIZATION AND HEPARIN

Recurrent emboli (<2 wks)
12% of untreated (2-22%)
5% of anticoagulated (0-5%)
Hemorrhagic complications (with Anticoagulation)
5% ( with deterioration)
14-20% (without deterioration)
Occur in 20% of large infarcts

OTHER STROKES,
IN OTHER FOLKS.

CEREBROVASCULAR DISEASE:

HYPERTENSIVE

Arteriolar Sclerosis

ARTERIOLOSCLEROSIS

Hyaline arteriolosclerosis
Hyperplastic arteriolosclerosis
"Lipohyalinosis"

HYPERTENSIVE CVD

Arteriolar occlusion - ischemia
(Lacunae, Binswanger)
Arteriolar rupture - hemorrhage
(Hematoma - BG, Thal., etc.)
Etat Crible (Dilated V-R)
(status cribrosus / cribalis)

Arteriolar Sclerosis

Spontaneous Arteriolar Occlusion
lacunar infarcts, Binswanger
Spontaneous Rupture
Ectatic Elongation
(status cribrosus / cribalis)
Etat Crible

HT BLEED

Ateriolar Sclerosis
Penetrating Vessels
Deep (Nuclear) Areas

HT HEMORRHAGE

Putamen 55%
Cerebrum 15%
Thalamus 10%
Pons 10%
Cerebellum 10%

INTRA-CEREBRAL HEMORRHAGE

Dense and Homogeneous
Round/oval shape
Basal ganglia/deep white
Proportional mass effect
Extension into ventricle
CHARCOT-BOUCHARD
MICRO-ANEURYSMS

Arteriolar Sclerosis

LACUNAE (Lacunar Infarcts)
Multiple
Small (1-15 mm.)
Deep (Putamen, Thalamus, Pons)
Pure Motor Hemiplegia
Arteriolosclerosis (HT)

WATERSHED INFARCTS

Hypotension, Shock, CPR
< 50mm Hg for > 10 min
Depths of Sulci
Boundary zones

SELECTIVE VULNERABILITY

Watershed/Boundary Zones
Hippocampus - Sommer's Sector
Globus Pallidus
Cerebellum
Cerebral III, IV, V

AMYLOID / CONGOPHILIC
ANGIOPATHY

AMYLOID ANGIOPATHY

Age > 65
Lobar Hemorrhage (Not BG)
Cortex, Subcortical WM
MULTIPLE Hemorrhages
Simultaneous
Metachronous