1/6. Fibrocartilaginous embolism--an uncommon cause of spinal cord infarction: a case report and review of the literature.Fibrocartilaginous embolism is a rare cause of spinal cord infarction. It is postulated that an acute vertical disk herniation of the nucleus pulposus material can lead to spinal cord infarction by a retrograde embolization to the central artery. An increased intradiskal pressure resulting from axial loading of the vertebral column with a concomitant valsalva maneuver is thought to be the initiating event for the embolus. We present a previously healthy 16-year-old boy with sudden onset of back pain and progressive paraparesis within 36 hours after lifting exercises in a squat position. His clinical presentation and neuroimaging studies were consistent with spinal cord infarction resulting from a central artery embolus at the T8 spinal cord level. Laboratory investigation showed no evidence of infectious, autoimmune, inflammatory, or neoplastic causes. Although no histologic confirmation was obtained, lack of evidence for other plausible diagnoses in the setting of his clinical presentation and in the magnetic resonance imaging findings made fibrocartilaginous embolism myelopathy the most likely diagnosis. We postulated that some cases of transverse myelitis might actually be fibrocartilaginous embolism, making it a more prevalent cause of an acute myelopathy than commonly recognized. Relevant literature and current theories regarding the pathogenesis of fibrocartilaginous embolism myelopathy are reviewed.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
2/6. Lacunar infarctions due to cholesterol emboli.BACKGROUND AND PURPOSE: hypertension is commonly considered the major cause of lacunar infarctions. However, in some cases, it has been suggested that lacunes could be caused by cerebral emboli from cardiac or carotid sources. cholesterol cerebral emboli have been rarely reported as a cause of lacunes. CASE DESCRIPTION: We describe a 79-year-old patient with a progressive multi-infarct dementia who developed transient motor aphasia and paresis of the right arm. Computed tomography showed lacunar infarcts in the right caudate nucleus, left thalamus, and left putamen, as well as an old right frontal infarction. Neuropathological examination demonstrated no prominent vascular hyalinosis, but did show multiple cholesterol emboli occluding small arteries around lacunar infarcts and leptomeningeal arteries near cortical infarcts. The cholesterol material presumably originated in the extended atheromatous changes along the aortic arch. CONCLUSIONS: Our report confirms that lacunes can be caused by cholesterol emboli in some patients. Small cerebral emboli should not be overlooked as a cause of lacunes.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
3/6. Possible role of collagen in transverse myelitis and chymopapain-induced paraplegia.We studied the effect of nucleus pulposus (NP) on platelet aggregation. Our in vitro experiments showed that NP extract produced platelet aggregation and the addition of collagenase to the NP extract abolished this response. It was further shown that chymopapain did not affect the activity of the extract. We assume that collagen is the active platelet aggregant in the NP extract. Intravascular release of collagen may cause platelet aggregation, vascular obstruction, ischemia, and cord necrosis in a patient with acute transverse myelitis. Intradiskal chymopapain is known to cause transverse myelitis and it is possible that collagen released during the action of the enzyme initiates a similar chain of events.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
4/6. Posterior paralysis due to fibrocartilaginous embolism in two weaner pigs.Acute posterior paralysis in two weaner pigs was attributed to ischemic infarction of the lumbar spinal cord due to fibrocartilaginous emboli. These arterial and venous emboli were assumed to have originated from the nucleus pulposus of one or more intervertebral discs. There was no indication of an initiating factor in either instance, although some form of trauma may have been involved. Lesions were not grossly evident and were limited to one or two lumbar segments. Although it appears to be a rare occurrence, fibrocartilaginous embolism of the spinal cord should be considered in cases of acute paralysis in pigs particularly when gross lesions are absent.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
5/6. natural history of spinal cord infarction caused by nucleus pulposus embolism.Nucleus pulposus embolism causing spinal cord infarction is exceptional. A 16-year-old girl was seen with sudden onset of interscapular pain and paraplegia from fatal ischemic transverse myelopathy due to arterial and venous occlusions by fibrocartilaginous embolism. In 32 cases of nucleus pulposus embolism, females predominated (69%) and age distribution was bimodal with peaks at 22 and 60 years (median, 38.5). Embolization was either arterial and venous (50%) or purely arterial (50%). Myelopathy predominated in cervical (69%) and lumbosacral (22%) segments. Schmorl's nodes, larger volume and vascularization of nucleus pulposus in the young, and spinal arteriovenous communications, trauma, and degenerative changes in older patients could be important pathogenetic factors. diagnosis requires histopathologic confirmation. Nucleus pulposus embolism may be an underlying cause in cases diagnosed as transverse myelitis and ischemic infarction of spinal cord.- - - - - - - - - - ranking = 6keywords = nucleus (Clic here for more details about this article) |
6/6. Fibrocartilaginous embolism of the spinal cord: a clinical and pathogenetic reconsideration.A 16 year old girl did a handstand for fun, returned to her feet, experienced a sudden pain in her back, and became progressively paraplegic within 30 hours. MRI showed lumbar cord swelling, multiple Schmorl's nodes, a collapsed T11-T12 disc space, and intraspongious disc prolapse into the T12 vertebral body. These findings, related to the initial manoeuvre, suggested that an acute vertical disc herniation could have occurred as the first step in a process leading to spinal cord infarction due to fibrocartilaginous emboli from the nucleus pulposus of the intervertebral disc. The medical literature so far reports 32 cases of fibrocartilaginous embolism (FCE) of the spinal cord, all at necropsy, with the exception of one histologically demonstrated in a living patient. A clinical diagnosis of FCE would be desirable for many important reasons, but was never made. This causes severe limitations in the knowledge of the disease and precludes any therapeutic possibility. On the basis of the clinical features and findings in the present case, compared with data from the reported cases, a first attempt is made to identify the clinical context within which new information obtainable through MRI examination can lead to a reliable clinical diagnosis of FCE. The vexed question of the pathogenesis has been reviewed. An increased intraosseous pressure within the vertebral body, due to acute vertical disc herniation, seems to offer a consistent pathogenetic explanation and some therapeutic prospects.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |