Photo 1a

Photograph 1a

Circle of Willis with severe atherosclerosis. Note the large fusiform aneurysm of the vertebral artery. Atherosclerosis of the intrinsic arteries of the CNS appears to follow systemic atherosclerosis by several years. When brain infarction is due to atherosclerotic occlusive disease the offending vessel is usually a major systemic artery such as the internal carotid. Intrinsic vessel disease, as in this patient, can directly cause cerebral infarction. It may also contribute to inadequate perfusion in situations where the delivery of oxygenated blood to the brain is compromised.

Photo 4

What microscopic features in this photograph, a section taken from Sommer’s sector of the hippocampus, allow you to determine that this is a good example of ischemic neuronal necrosis perhaps due to a severe drop in systemic perfusion. How old is this lesion? 12-24 hours, several days, weeks to months. Why? Can you invoke another clinical setting in which this population might be selectively destroyed? Can you link excititory amino acid receptor overdrive to this process. Try to be specific concerning receptor types, and mechanisms of cell death.

Photo 3 & Photo 5

These slides depict acute cerebral infarction. What vessel(s) was compromised in photographs 3 and 5. Is the compromise proximal, at the main proximnal branching point or distal. You can easily seen the herniation of the cingulate gyrus in the acute examples. Whenever there is a substantial increase in the mass of the intracranial tissues, as in extensive acute infarction, transtentorial herniation of the uncus and or transforamen magnum herniation of the cerebellar tonsils may occur. These are life threatening. How?

For more information on cerebral herniation go to Section 4 - Alcohol Trauma and Transtentorial Herniation.

Photo 5a & Photo 5b

These photographs show the gross evolution of a cerebral infarction from a subacute lesion with some tissue removal (on the left side) to old cavitary lesions (on the right side). Note that the unfortunate patient with the old lesions sustained infarctions of both middle cerebral territories. In contrast to systemic tissues, brain infarction, a form of liquificative necrosis, results in cavitary lesions.

Photo 6

The photograph on the left depicts a sharply delineated area of infarction (encephalomalacia). How old is this lesion and what vascular territory is it in. In contrast, the photo on the right shows this patient had an infarctions in a watershed pattern between anterior and middle cerebral vessels. Compare the lesion on the left with those in photographs 3 and 5 above, which depict very acute infarctions.

Photo 10

Photograph 10 pons-compare this lesion with those in 3,5 and 6 above. This is an example of old cavitary infarction. The lesion may be call a lacunae. This is an example of infarction consequent to disease of small medial perforating vessels, in this instance medial perforating branches of the basilar artery. What systemic factors are important in patients with this pattern of disease? Another part of the brain which is vunerable in this setting, is shown on the right side. Do you understand why hypertensive hemorrhages have a similar pattern of distribution. Can you picture the microvascular microscopic finding in each of these circumstances? In which do you expect micrcharcot aneuerysms and fibrinoid change?

Photo 15

Photograph 15 is of a hemorrhagic infarction. Why is this not a hypertensive hemorrhage. Hemorrhagic infarctions are often associated with systemic emboli. Note the friable vegetations of the aortic valve shown in photograph 11. You can image how a single large fragment might enter the systemic cirrculation and impact within a branch of a cerebral artery to cause this infarction. In contrast, a shower of smaller fragments could travel to the more distal cerebral cirrculation to produce multiple small infarctions at the cortical grey white margins.

Photo 17 & Photo 18

Photographs 17 and 18 show acute, massive hypertensive hemorrhages. Contrast these images with that depicted in 15. Note that the blood here is under enough driving pressure to destroy the tissue, rupture through the ependymal lining and fill the ventricle with blood. When massive, these tend to be fatal events. What is the pathogenesis of this type of hemorrhage? What simple procedure and subsequent therapy is protective?

Photo 18a & Photo 18b

Photographs 18a & 18b show arteriolar changes, associated with severe diastolic hypertension, which could result in arteriolar rupture and parenchymal hemorrhage. Click on the image for the diagnosis.

Photo 21 & Photo 22

Photographs 21 and 22 are of Berry Aneurysms. Rupture of these is an important cause of subarachnoid hemorrhage. What other problems or presentations do they have. What is their pattern of distribution.