Strokes: Extracranial ICA
Diagrams
Extracranial Internal Carotid Artery (ICA)
The mechanism of occlusion of the extracranial ICA is almost always formation of thrombus on an ulcerated atherosclerotic plaque located at or near the carotid bifurcation. Sometimes embolism from a cardiac source or carotid dissection is responsible, but this is quite rare. The clinical syndromes that result are variable--they range from total infarction of the entire cortical and deep territory of the middle cerebral artery (MCA) and anterior communicating artery (ACA) affecting most functions of one entire hemisphere to a small cortical MCA territory infarction to no neurologic deficit whatsoever. This incredible variability reflects what sources of collateral flow are available and how much blood the collaterals actually carried in the particular patient at the time of occlusion.
| Question: |
| Can you think of three places where anastamotic flow might be established that could nourish carotid territory if the ICA were occluded slowly and progressively, allowing enough time for collaterals to increase their diameter and hence the amount of blood they carry? |
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With all this variability in clinical presentation, you may be wondering how physicians come to suspect an ICA occlusion. The answer is often in the patient's past and present medical history.
Clues include:
- repeated transient ischemic attacks always in carotid territory
- a carotid bruit or direct evidence of stenosis from angiography or
- ultrasound studies showing reversed blood flow in ophthalmic artery branches.
| Question: |
| If there is a functional anastamosis between external and internal carotid using ophthalmic artery branches, what direction would the blood be flowing? |
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