MCA infarct

Discussion :
Acute Ischemic Infarction
Histo:cortical cytotoxic edema (from loss of vascular autoregulation) followed by white matter vasogenic edema

(a)Substage I(12-24 hours)
NCCT
-lowe density basal ganglia
-effacement of gray-white matter junction, eg, "insular ribbon sign" hypodense extreme capsule no longer distinguishable from insular
-subtle sulcal effacement (8%)

CECT:
-no iodine accumulation in affected cortical

MR :
(routinely positive by 4-6 hours post ictus):
-subtle narrowing of sulci
-increase in thickness of cortex (= gyral swelling)
-blurring of gray-white matter junction on T2- and proton-density images
-contrast-enhanced cortical arterial vessels in area of brain injury (due to slow arterial blood flow provided by collateral circulation via leptomeningeal
-subtle low-signal intensity on T1WI, high-signal intensity on T2WI (masking of gyral infarcts on heavily T2WI due to sulcal CSF intensity)

MRA:
-absence of flow for infarcts >2 cm in diameter

(b)StageII (1-7 days)
NCCT:
-hypodense wedge-shaped lesion with base at cortex in a vascular distribution (in 70%) due to vasogenic + cytotoxic edema
-mass effect (23-75%): sulcal effacement, transtentorial herniation, displaced subarachnoid cisterns + ventricles
-"bland infarct" may be transformed into hemorrhagic infarct after 2-4 days (due to leakage of blood from ischemically damaged capillary endothelium following lysis of intraluminal clot + arterial reperfusion)

CECT:
-gyral enhancement along cortex

MR:
-intravascular enhancement sign (77%) = Gd-pentetate enhancement of vessels supplying infarct after 1-3 days
-meningeal enhancement sign = Gd-pentetate enhancement of meninges adjacent to infarct after 2-6 days

Angio:
-narrowed / occluded vessels supplying the area of infarction
-delayed filling + emptying of involved vessels
-early draining vein
-luxury perfusion of infarcted area (rare) = loss of small vessel autoregulation due to local increase in pH