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.