cerebral ischemia
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CT Imaging ofCT Imaging of
Cerebral Ischemia Cerebral Ischemia and Infarctionand Infarction
Presented by EKKASIT SRITHAMMASIT, MD.Presented by EKKASIT SRITHAMMASIT, MD.
Ann G.Osborn Diagnostic Neuroradiology; 11: 341-369
IntroductionIntroduction
Stroke is a lay term that encompasses a heterogeneous group of cerebrovascular
disorders .
The four major types of stroke : • Cerebral infarction (80%)• Primary intracranial hemorrhage (15%)• Nontraumatic subarachnoid hemorrhage (5%)• Miscellaneous – vein occlusion (1%)
Cerebral InfarctionCerebral Infarction
• Large vessel occlusions ( ICA, MCA, PCA) – 40-50%
• Small vessel (lacunar) infarcts – 25%
• Cardiac emboli – 15%
• Blood disorders – 5%
• Nonatheromatous occlusions – 5%
Table of contentTable of content
• Pathophysiology• CT Imaging of Cerebral Infarcts:
Overview• Acute Infarcts• Subacute Infarcts• Chronic Infarcts• Lacunar Infarcts• Hypoxic-Ischemic Encephalopathy
PathophysiologyPathophysiology
Physiology Physiology of cerebral ischemia and of cerebral ischemia and
infarctioninfarction
**Most common situation**
Densely ischemic central focus
Less densely ischemic “penumbra”
Physiology Physiology of cerebral ischemia and of cerebral ischemia and
infarctioninfarction
Physiology Physiology of cerebral ischemia and of cerebral ischemia and
infarctioninfarction **Ischemia produces**
Biochemical Reactions
Loss of ion homeostasis, Osmotically obligated water, anaerobic glucolysis
Loss cell membrane function & Cytoskeletal integrity
Cell death
Physiology Physiology of cerebral ischemia and of cerebral ischemia and
infarctioninfarction
**Selective vulnerability**
Most vulnerable = NeuronMost vulnerable = Neuron
Follow by Astrocytes, oligodendroglia, microglia and endothelial cells
Physiology Physiology of cerebral ischemia and of cerebral ischemia and
infarctioninfarction
**Collateral supply**
Dual or even triple interdigitating supplyDual or even triple interdigitating supply : : Subcortical white matter U-fiber, external capsule, claustrum
Short arterioles from a single sourecShort arterioles from a single sourec : The cortex : The cortex
Large, long, single source vesselsLarge, long, single source vessels : Thalamus, basal : Thalamus, basal ganglia, centrum semiovaleganglia, centrum semiovale
Physiology Physiology of cerebral ischemia and of cerebral ischemia and
infarctioninfarction
Border zonesBorder zones / Vascular watershed/ Vascular watershed
• Arterial perfusion pressure is lowest in these zone because of arteriolar aborization
• The first to suffer ischemia and infarction during generalized systemic hypotension
Border zones / Vascular Border zones / Vascular watershedwatershed
Adult, term infants Fetus, preterm infant
Cortex and cerebellum Deep periventricular region
CT Imaging of Cerebral CT Imaging of Cerebral InfarctsInfarcts
CT Imaging of Cerebral CT Imaging of Cerebral InfarctsInfarcts
The imaging The imaging manifestations of manifestations of cerebral ischemia cerebral ischemia varyvary significantly significantly
with timewith time
Acute InfarctsAcute Infarcts
Acute InfarctsAcute Infarcts
The role of immediate CT The role of immediate CT in the management of acute cerebral infarction is two foldin the management of acute cerebral infarction is two fold
1.1. Diagnose or exclude intracerebral Diagnose or exclude intracerebral hemorhagehemorhage
2.2. Identify the presence of an Identify the presence of an underlying structural lesion such as underlying structural lesion such as tumor, vascular malformation.tumor, vascular malformation.
Acute InfarctsAcute Infarcts
First 12 hoursFirst 12 hours
• Almost 60 % = Normal
• Hyperdense artery (25 – 50%)
• Obscuration of lentiform nuclei
12 – 24 hours12 – 24 hours
• Loss of gray-white interfaces ( insular ribbon sign)
• Sulcal effacement
Acute InfarctsAcute Infarcts
Hyperdense arteryHyperdense artery
• Usually the MCA – hyperdense MCA sign (25% of unselected acute infarct)
• Hyperdense MCA sign 35-50% of MCA stroke
• Caused by acute intraluminal thrombus
Acute InfarctsAcute Infarcts
Hyperdense MCA
Acute InfarctsAcute Infarcts
Obscuration of lentiform nuclei
Acute InfarctsAcute Infarcts
Loss of gray-white interfaces ( insular ribbon sign)
Acute InfarctsAcute Infarcts
Sulcal effacement
Subacute InfarctsSubacute Infarcts
Subacute InfarctsSubacute Infarcts
1-3 days1-3 days
• Increase mass effect
• Wedge-shaped low density area that involves both gray and white matter
• Hemorrhagic transformation (basal ganglia and cortex are common sites)
4-7 days4-7 days
• Gyral enhancement
• Mass effect, edema persist
Subacute InfarctsSubacute Infarcts
Subacute InfarctsSubacute Infarcts
Subacute InfarctsSubacute Infarcts
Subacute InfarctsSubacute Infarcts
ECCT
Chronic InfarctsChronic Infarcts
Chronic InfarctsChronic Infarcts
Months to yearsMonths to years
• Encepholomalacic change, volume loss
• Calcification rare
Chronic InfarctsChronic Infarcts
Lacunar InfarctsLacunar Infarcts
Lacunar InfarctsLacunar Infarcts
• Small deep cerebral infarcts
• Typically located in the basal ganglia and thalamus
• Small infarcts are often multiple
• Most true lacunar infarcts are not seen on CT
• Present they are usually seen as part of more extensive white matter disease
Lacunar InfarctsLacunar Infarcts
Lacunar InfarctsLacunar Infarcts
Hypoxic-Ischemic Hypoxic-Ischemic EncephalopathyEncephalopathy
Hypoxic-Ischemic Hypoxic-Ischemic EncephalopathyEncephalopathy
• Consequence of global perfusion or oxygenation disturbance
• Common causesCommon causes – severe prolonged hypotension, cardiac arrest with successful resuscitation, profound neonatal asphyxia, cabonmonxide inhalation ( Decrease CBF)
• May be caused by RBC oxygenation is faulty
• Two basic patterns: “border zone infarcts” and “generalized cortical necrosis”
Border zones / Vascular Border zones / Vascular watershedwatershed
Adult, term infants Fetus, preterm infant
Cortex and cerebellum Deep periventricular region
Hypoxic-Ischemic Hypoxic-Ischemic EncephalopathyEncephalopathy
• The most frequently and severely affected area is the parietooccipital region at the confluence between the ACA, MCA, and PCA territories.
• The basal ganglia are also common sites
• In premature infants HIE manifestations are those of periventricular leukomalacia
• Most common observed on NECT is a low density band at the interface between major vascular territories.
• The basal ganglia and parasagittal areas are the most frequent sites.
At 2 months of age, T1-weighted brain MR imaging shows high-signal regions in the periventricular area, atrophy of the white matter and serrated ventricular walls.
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