The pathogenic process leading from the development of the cerebrovascular or extracranial
atherosclerosis of the occurrence of acute ischaemic stroke and consequent cell damage is complex, and many of
the intermediary damage is complex, and many of the intermediary steps are not completely understood.
Ischaemic stroke may arise from the atherosclerotic large cerebral arteries (eg, carotid, middle cerebral, and basilar
arteries) or atherosclerotic small cerebral arteries (eg, lenticulostriate, basilar penetrating, and medullary arteries);
ischaemic stroke may also be cardioembolic in origin.� Most investigations of atherogenesis have focused on the coronary
arteries, but, with some possible exceptions, similar processes occur in the cerebral circulation.� In the brain, the
process is better characterized in the larger arteries than in small arteries supplying deep cerebral white matter.�
Some evidence suggests that the underlying pathogenetic process in small arteries may differ from that described in
larger arteries.
Atherogenesis is a decades-long process in which the lumen of a blood vessel becomes narrowed by cellular and
extracellular substances to the point of obstruction. An autopsy study of coronary arteries and aortas in 1,160 people
who died between full-term birth and age 29 years found that the earliest lesion of atherosclerosis is the fatty streak.
Approximately 65% of children between ages 12 and 14 years had such lesions.�Fatty streaks, which are grossly visible as
areas of yellowish discoloration of the surface of the intimal layer of the vessel wall, are widely distributed throughout
the coronary arterial vasculature.�On microscopy, the lesions primarily consist of lipid-filled macrophages (foam cells).
The autopsy study revealed that an additional 8% of children in late childhood or early adolescence had progressed beyond
the fatty-streak stage and had developed more advanced, focal lesions.� These lesions, which occur only in areas of
eccentric thickening (eg, at branch points of the arterial vessel), are characterized by the addition of massive
extra-cellular lipids that displaced normal cells and matrix.
In the third decade of life, some atheromatous lesions evolve into complicated fibrous plaques, consisting of a central
acellular area of lipid covered by a cap of smooth muscle cells and collagen.� Caps tend to form slowly at first, but
with deposition of platelets and fibrin on the surface - which appears to be the result of endothelial injury - the caps
thicken quickly, possibly as a result of thrombosis-dependent fibrotic organization.
The progression of early atherosclerotic lesions to clinically relevant advanced atherosclerotic lesions occurs with
increased frequency in persons with risk factors for atherosclerotic disease (eg, hypercholesterolaemia, hypertension,
cigarette smoking).
References:
DeGraba et al.� In Barnett et al. (eds.) 1992: 29.
Breslow JL. Science 1996; 272: 685.
Stary HC. Atherosclerosis 1989; 9 (Suppl 1): 119.
Pathogenic Process - Vascular Occlusion by Platelet Aggregates
The picture depicts vascular occlusion by platelet aggregates, as a result of a lesion or
atherosclerosis of the endothelium.
Drugs that prevent platelet over-reactivity help to prevent this kind of arterial occlusion in the brain or in the heart.
References:
M�ller. 1997
Pathogenic Process - Platelets with Pseudopods
When the endothelium is subjected to insult, platelets respond by losing their discoid form and developing pseudopodia. The pseudopodia interconnect and the platelets adhere to the injured area.
References:
Nilsson. 1984
Pathogenic Process - Surface of a Thrombus
Red blood cells and platelets become enmeshed in the fibrin network produced by the clotting mechanism. The result is the formation of a thrombus, which cannot be easily broken down.
References:
Nilsson. 1984
Pathogenic Process - Occluding Thrombus
As the thrombus increases in size, it projects into the lumen of the vessel and obstructs blood flow. Emboli may become detached and cause vascular obstruction at a site distant from the original thrombus. This photograph shows the interior of the femoral vein with an occluding thrombus discovered at autopsy. The patient died as a result of a stroke.
References:
Nilsson. 1984 |
