Mini Robbins Pathology Pdf
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A wide range of other ultrastructural abnormalities have been recognized in CADASIL. In the brain and retina of CADASIL patients, the laminar parenchyma contains granular degeneration of cortical and subcortical neurons, and confluent vessel wall thickening with reduction of laminations and necrosis are the main pathologic findings. Pathological findings in the brain and spinal cord are characterized by focal degeneration of the central and peripheral nervous system, and even sometimes generalized degeneration, despite the absence of any clinical or radiologic evidence of central nervous system involvement. The pathological hallmark of CADASIL is the presence of granular osmiophilic material (GOM) in the media and internal elastic lamina of small- and medium-sized cerebral, spinal and retinal arteries, arterioles, and venules (Fig. 2). GOM is a granular substance that is composed of amorphous eosinophilic material and fibrils with an electron-dense core, and is similar to amyloid plaques (Fig. 1). GOM was first described in CADASIL and in patients with familial cerebral amyloid angiopathy (FCAA) [180,181]. In the brain and retina of CADASIL patients, GOM accumulates in the vascular wall of medium and small arteries, arterioles, and venules (Fig. 2). GOM also accumulates in small arteries of FCAA patients, but not in those of hereditary cerebral hemorrhage with amyloidosis (HCHWA-D) patients [182]. The GOM-positive lesions in CADASIL and FCAA patients are characterized by the presence of amyloid-like material in the wall of small- and medium-sized vessels. Also, these patients exhibit a vasculopathy, characterized by intimal thickening, with or without an obliterative or calcified endarterectomy lesion (Fig. 2). Intimal thickening in CADASIL or FCAA is most often observed in large vessels of the brain and retina (Fig. 2). In contrast, vascular thickening is occasionally found in the mid-sized vessels in CADASIL or FCAA. The exact pathogenesis of GOM is not clear. The typical lesions are probably degenerative, and no evidence of inflammatory or immunologic changes has been reported. Therefore, the presence of GOM is not likely caused by an immune-mediated process [181,183].
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