圖片說明

圖片說明

History :
This 40 y/o gentleman suffered from sudden onset of eneral weakness, conscious disturbance

CECT: -gyral enhancement along cortexImage finding :
-Hyperintense area on T2WI, FLAIR and DWI at territory of right
MCA,involving right BG and T-F region consistent with recent infarct.
-Hemorrhage transformation with patechial hemorrhage or laminar necrosis is noted.
-Relatively small caliber of M2 branch of right MCA.

Diagnosis :
Right MCA infarct

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

  1. 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
  2. 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