ATHEROSCLEROSIScauses 90% of thromboembolic disease & vascular stenosis
1. Etiology – focal endothelial change or subtle injury allows LDL & macrophage into intima Smooth muscle cells recruited & filled with fatty esters – foam cells. Fibrotic cap covers core of dead foam cells .Associated inflammation allows granulation tissue & neovascularity. Plaques ,hematoma & necroses acts as nidus for thrombi
2. Imaging – angio remains gold standard, US, CT & MRA alsoUS – peak systolic velocity best parameter for assesing stenosis . Angio done to – 1) determine degree of stenosis & ulceration 2) Identify tandem lesions in siphon or intracranialy 3) evaluate existing or potential collateral circulation. CT – identifies vessel ectasia & mural calcification .MRI – flow voids do not exclude significant stenosis
3. Carotid Origin Stenosis – endarterectamy helps if 70-99% delayed veiws show “string sign” of high grade stenosis.
4. Tandem Lesion – distal stenosis of carotid also seen in 2%hemodynamic effect additive, usually in siphon, PTA needed
5. Collateral Circulation – critical severe stenosis or occ circle of willis #1, complete in only 25%patent anterior communicating artery usually adequate to allow clamping external carotid to ophthalmic good, few others adequate
6. Subclavian Steal – occulusion of proximal subclavian or arch, irregular flow reversed in vertebral artery to supply arm & shoulder. Atherosclerotic Diseases can effect any proximal great vessel or arch
CEREBRAL ISCHEMIA AND INFARCTION
1. Physiology – central & peripheral portions differ. Central nidus quickly irretrievably damaged this is the zone of frank Cerebral Infarction. Penumbra – peripheral cells viable but at risk for hours. Zone of generalized neuronal necrosis, support cells left . Selective neuronal necrosis – only most vulnerable neurons. Ion homeostatsis lost: C++, Na+, & Cl- accumulate. Anerobic glucolysis causes metabolic acidosis. Free Radicals accumulate, cytoskeleton breaks down, cell dies
2. Selective Vulnerability – sensitivity to ischemia varies. Neurons most vulnerable are astrocytes, oligodendrocytes, microglia, Hippocampal pyramidal fibres most sensitive of the neurons. Neocortical layers III, V & VI, purkinje & neostriatum, Thalmus, Basal Ganglia, Centrum Semiovale susceptable ,long single arteriole vulnerable to anoxia & hypoperfusion. Vascular Watersheds – cortex & Cb in adults & term infants in deep perventricular region in premature babies. Adults – occurs in the WM near caudate or frontoparital Hyperacute Infarcts –
Acute Infarcts – 12-48hrsCT – sulcal effacement, low density basal ganglia, Gray-White interface lost – Insular ribbon sign. MRI – Hyperintensity on T2 develops in 8hrs associated with mass effect in 25%, usually mild, maximum at 5 days. Meningeal enhancement adjacent to infarct
5. Subacute Infarcts – 2 days – 2wks CT – 24-48hrs wedge shaped area of low attenuation visible. Edema & mass effect increases initially, subsides by 4-7 days. hemorrhagic transformation at 1-3 days, .Contrast enhancement from BBB breakdown, gyral or RING develops at 3-4 days & can last 8-10 wks, 20% seen only with a contrast scan, but NOT good for Pt . MRI – meningeal & intravascular enhancement decreases at 2-4 days. parenchymal enhancement begins & can last for weeks. T2 begins to fade as protiens from cell lysis spill out, 1-2 wks – T1 post-contrast striking, T2 NormalWallerian Degeneration – hypodense band in corticospinal tract
6. Chronic Infarcts – > 2 weeks. Gliosis & volume loss are hallmark of stroke residua. Both CT & MRI show well delineated encephalomalacia. Ipsilateral ventricle enlarges, dystrophic calcification rare. Hemmorhagic areas develop predictably
7. Lacunar Infarcts – 25% of all strokes, basal ganglia & thalami mostly affected. single long penetrating vessel to deep cerebral gray matter. CT – usually only seen with associated WM disease. MRI – dec T1, Inc T2 – DDx – subependymal myelin palloror ,Virchow-Robin – enlarged perivascular spaces
8. Hypoxic-Ischemic Enchephalopathy – global rather than focal. Etiology is prolonged hypotension, asphyxia, or CO poisoning.Basal Ganglia & border zones most sensitive.
Pseudolaminar Necrosis – Generalized cortical ischemia. layers III, V & VI effected along with caudate & putamen9.
Hemorrhagic Infarcts – easily detected by CT& MRI – standard images have poor sensitivty
10. Cerebellar Infarcts– rare due to extensive collarterals. Present with Vertigo, ataxia, nausea & vomiting. 90% occur in PICA distribution, congenital abscence. 25% enhance, most at subacute, gyral or ring type CT Finding Summary – Normal up to 24hrs. Peak mass effect at 2-5d, gone by 2nd week, Peak enhancement in 2nd week, predominately gray matter.