In advanced plaques, the central core of the plaque usually contains extracellular cholesterol deposits (released from dead cells), which form areas of cholesterol crystals with empty, needle-like clefts. At the periphery of the plaque are younger "foamy" cells and capillaries. These plaques usually produce the most damage to the individual when they rupture. Cholesterol crystals may also play a role. The fibrous plaque is also localized under the intima, within the wall of the artery resulting in thickening and expansion of the wall and, sometimes, spotty localized narrowing of the lumen with some atrophy of the muscular layer. The fibrous plaque contains collagen fibers (eosinophilic), precipitates of calcium (hematoxylinophilic), and rarely, lipid-laden cells.In effect, the muscular portion of the artery wall forms small aneurysms just large enough to hold the atheroma that are present. The muscular portion of artery walls usually remains strong, even after they have remodeled to compensate for the atheromatous plaques.However, atheromas within the vessel wall are soft and fragile with little elasticity. Arteries constantly expand and contract with each heartbeat, i.e., the pulse. In addition, the calcification deposits between the outer portion of the atheroma and the muscular wall, as they progress, lead to a loss of elasticity and stiffening of the artery as a whole.The calcification deposits, after they have become sufficiently advanced, are partially visible on coronary artery computed tomography or electron beam tomography (EBT) as rings of increased radiographic density, forming halos around the outer edges of the atheromatous plaques, within the artery wall.
Organic causes of amnesia can be difficult to detect, and often both organic cause and psychological triggers can be entangled. Failure to find an organic cause may result in the diagnosis that the amnesia is psychological, however it is possible that some organic causes may fall below a threshold of detection, while other neurological ails are thought to be unequivocally organic (such as a migraine) even though no functional damage is evident. Possible malingering must also be taken into account. Some researchers have cautioned against psychogenic amnesia becoming a "wastebasket" diagnosis when organic amnesia is not apparent. Other researchers have hastened to defend the notion of psychogenic amnesia and its right not to be dismissed as a clinical disorder. Diagnoses of psychogenic amnesia have dropped since agreement in the field of transient global amnesia, suggesting some over diagnosis at least. Speculation also exists about psychogenic amnesia due to its similarities with pure retrograde amnesia, as both share similar retrograde loss of memory. Also, although no functional damage or brain lesions are evident in the case of pure retrograde amnesia, unlike psychogenic amnesia it is not thought that purely psychological or psychogenic triggers are relevant to pure retrograde amnesia. Psychological triggers such as emotional stress are common in everyday life, yet pure retrograde amnesia is considered very rare. Also the potential for organic damage to fall below threshold of being identified does not necessarily mean it is not present, and it is highly likely that both psychological factors and organic cause exist in pure retrograde amnesia.