The internal elastic lamina in the basilar artery and its possible significance for intimal thickening

Apmis ◽  
1991 ◽  
Vol 99 (7-12) ◽  
pp. 773-779
Author(s):  
K. Heldal ◽  
E. Svendsen ◽  
B. O. MaeEhle
Apmis ◽  
1996 ◽  
Vol 104 (1-6) ◽  
pp. 395-400 ◽  
Author(s):  
OTSO JÄRVINEN ◽  
TERO SISTO ◽  
JARI LAURIKKA ◽  
MATTI TARKKA

2021 ◽  
Vol 12 ◽  
pp. 4
Author(s):  
Yoshimichi Sato ◽  
Kuniyasu Niizuma ◽  
Hideki Ota ◽  
Hidenori Endo ◽  
Teiji Tominaga

Background: Chronic basilar artery dissection (BAD) is a rare pathology, and only a few reports have been mentioned in the literature. The imaging features of chronic BAD, especially those that develop into a subarachnoid hemorrhage (SAH), are unknown. Case Description: We report a unique case of a chronic BAD with a split intimal flap that developed into an SAH. A 74-year-old man was diagnosed with BAD. After considering all treatment options, conservative treatment was selected for the patient. We continued imaging follow-up of the patient in our outpatient clinic once a year. The BA gradually dilated and the internal flap split. The patient and his family refused surgical treatment; therefore, conservative treatment was continued. Six years and 2 months from the first diagnosis, he developed a massive SAH and died. Conclusion: In the case of this patient, the weakened condition of the internal elastic lamina may have caused dissection of the intimal flap between the intima and media. Furthermore, the dissection may have developed and connected the true lumen to the pseudolumen and induced BA rupture. Thereby, split of the internal flap could be a risk factor for rupture in chronic BAD.


Author(s):  
A. Trillo

There are conflicting reports regarding some fine structural details of arteries from several animal species. Buck denied the existence of a sub-endothelial space, while Karrer and Keech described a space of variable width which separates the endothelium from the underlying internal elastic lamina in aortas of aging rats and mice respectively.The present communication deals with the ultrastrueture of the interface between the endothelial cell layer and the internal elastic lamina as observed in carotid arteries from rabbits of varying ages.


2020 ◽  
Vol 1 ◽  
pp. 247
Author(s):  
Derek Afflu ◽  
Dylan D. McCreary ◽  
Nolan Skirtich ◽  
Kathy Gonzalez ◽  
Edith Tzeng ◽  
...  

1952 ◽  
Vol 98 (411) ◽  
pp. 280-286 ◽  
Author(s):  
R. Vereker

Temporal arteritis, also called giant cell arteritis, or cranial arteritis, was first described in 1932 by Horton and Magath. This syndrome is caused by a reversible inflammation of the cranial arteries, especially the temporal arteries (which are visibly inflamed), causing headache, mental and neurological disturbances as well as general toxic signs, and almost always occurring after the age of fifty-five years.Pathology.—In the arteries involved there is a subacute inflammation of the adventitia and media with focal necrosis of the media, fragmentation and destruction of the internal elastic lamina with gross hypertrophy of the intima, often leading to occlusion of the vessel. In many cases giant cells are found in the media. Besides the cranial arteries other vessels are sometimes involved, e.g., the carotids (Scott and Maxwell 1941; Gilmour 1941), subclavian, coronary and femoral arteries (Cookeet al., 1946), post-auricular (Dick and Freeman 1940).Aetiologyis unknown. There is no evidence of tuberculosis or syphilis. A low-grade bacterial or virus infection of the arteries has been postulated, but repeated bacteriological examinations of the biopsied arteries have failed to isolate any organisms. The predilection which the condition shows for the temporal and cranial arteries is unexplained.


Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Yusuke Shimoda ◽  
Naoki Nakayama ◽  
Masaaki Hokari ◽  
Takeo Abumiya ◽  
Hideo Shichinohe ◽  
...  

Background and Purpose: Although recent researches on cerebral aneurysms (CAs) have been performed with the hydrodynamic or the molecular biological technique, the mechanisms of rupture are not fully understood. The aim of this study is to assess the mechanism by a comparison between ruptured and un-ruptured CAs with histopathological and electron-microscopic analysis. Methods: We analyzed 33 CAs (24 ruptured, 9 un-ruptured) collected surgically after neck clipping. As for the ruptured CAs, we operated them within 24 hours from the onset. HE staining, Elastica Masson staining, PTAH staining, and CD68 immunohistochemical staining were performed with paraffin sections. Morphological analysis with Scanning Electron Microscopy (SEM) was performed with 6 CAs (3 ruptured, 3 un-ruptured). Results: The common histopathological finding in both ruptured and un-ruptured CAs was that the aneurysmal wall consisted mostly of thick collagen layer without normal internal elastic lamina and media. The characteristic histopathological finding in ruptured CAs was inside intramural thrombus formation with infiltration of CD68 positive cells at the rupture point. The common SEM finding in both ruptured and un-ruptured CAs was the denudation of endothelial cells and the exposure of a subendothelial amorphous or a fibrous surface. The characteristic SEM finding in ruptured CAs was the cluster formation of thick fibrin fibers with incorporation of macrophages and platelets. Conclusions: While the endothelial denudation, the disappearance of internal elastic lamina and media, and the predominance of collagen layer in the aneurysmal wall were common in both ruptured and un-ruptured CAs, inside intramural thrombus formation with inflammatory reactions was characteristic only in ruptured CAs. This result suggests that thrombo-inflammatory reactions in CAs may act as a trigger for ruptures.


2011 ◽  
Vol 300 (2) ◽  
pp. H423-H430 ◽  
Author(s):  
Yasumi Uchida ◽  
Yasuto Uchida ◽  
Akimasa Matsuyama ◽  
Atsushi Koga ◽  
Yuko Maezawa ◽  
...  

Although there are a number of studies on vasospastic angina, the structural changes at the cellular level that occur in the coronary arterial wall during spasm are not well known. Coronary spasm was induced by brushing the coronary adventitia in nine anesthetized beagles, and structural changes in the spastic coronary segments were examined by light and electron microscopy, making comparisons with the adjacent nonspastic segments. The % diameter stenosis of the spastic segments as measured angiographically was 79.4 ± 12% (mean ± SD). Light microscopic changes in the spastic and nonspastic segments were as follows: medial thickness 1,512 vs. 392 μm ( P < 0.0001) and % diameter and % area stenoses of spastic segment 81.0% and 96.5%, respectively, indicating that spasm was induced by medial thickening. Circular smooth muscle cells (SMCs) in the media were arranged in parallel with the internal (IEL) and external (EEL) elastic lamina in nonspastic segments but radially rearranged in spastic segments. SMCs were classified by their patterns of connection to IEL into six types by electron microscopy. Of these, three contracted and pulled the IEL toward the EEL, causing folding of the IEL and waving of EEL resulting in thickening of the media and narrowing of the lumen. We conclude that coronary spasm was elicited by radial rearrangement of the medial SMCs due to their own contraction and resultant medial thickening and folding of IEL, creating a piston effect to narrow the lumen, i.e., spasm.


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