Coronal section of nasal cavities.




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 Stealocculusion 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

7. Intracranial Atherosclerotic Disease – irregular lumen & stenosis can lead to tortuous vessels & fusiform aneurysms
Basal ganglia disease

Basal Ganglia Hemorrhage Horizontal


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.