Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study is presented to promote prophylactic operation to prevent rebleeding after subarachnoid hemorrhage (SAH) of unknown cause. Twenty-two cases of nontraumatic SAH of unknown cause of a total of 254 cases of SAH treated during a 5-year period (1980-1984) were available for this study. A follow-up study (4 to 61 months after treatment; median, 43 months) revealed a 4.5% mortality rate. Four patients chosen from among the 22 SAH cases underwent prophylactic operation. The decision to operate was based on repeated angiography showing regional cerebral vasospasm corresponding to a limited hyperdense area on the computed tomographic scan at the time of the onset of SAH. Microsurgery revealed a minute protrusion (less than 2 mm in diameter) or thinning of the arterial wall with old hematoma of the surrounding brain in all 4 cases, and treatment required only coating of the abnormal site. All 4 patients are now fully recovered. Frequently, abnormal changes of such cerebral arteries as the anterior communicating artery, the internal carotid artery (C-1 and C-2), and the middle cerebral artery (M-1) may occur. Therefore, the authors emphasize the necessity of surgical treatment for specific cases of SAH with an unknown cause.
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PMID:Prevention of rebleeding after operation for subarachnoid hemorrhage of unknown cause. 408 Jan 28

This report describes a new and reliable technique for producing experimental noncommunicating syringomyelia. In 30 rats, 1.2 to 1.6 microliters of kaolin was microinjected into the dorsal columns and central gray matter of the spinal cord at C-6. The inoculations caused transient neurological deficits in four animals and no deficits in 26 animals. Within 24 hours, kaolin and polymorphonuclear leukocytes entered the central canal and drained rostrally. The clearance of inflammatory products induced a proliferation of ependymal cells and periependymal fibrous astrocytes, which formed synechiae and obstructed the canal at the level of injection and at one or more levels up to C-1. In 22 animals followed for 48 hours or longer, the upper end of the central canal became acutely dilated and formed an ependyma-lined syrinx that enlarged to massive dimensions within 6 weeks. The rostral syrinxes did not communicate with the fourth ventricle and were not associated with hydrocephalus. The histological findings in acute noncommunicating syringomyelia were characterized by progressive stretching and thinning of the ependyma, elongation of intracanalicular septae, and the formation of periependymal edema. After 3 weeks, there was progressive compression of the periependymal tissues associated with stretching of axons, fragmentation of myelin sheaths, and the formation of myelin droplets. These findings and the sequence in which they evolved were identical in most respects to those occurring in acute and subacute noncommunicating hydrocephalus.
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PMID:Noncommunicating syringomyelia following occlusion of central canal in rats. Experimental model and histological findings. 842 Dec 10