Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019270 (hernia)
 15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied the clinical picture of lumbar osteochondritis in 1,020 patients, 151 of whom were operated on. The monoradicular syndrome was diagnosed in 68%, the biradicular (involvement of two radicles) in 27%, and the polyradicular (involvement of three and more radicles) in 7% of the patients. In the authors' opinion, the development of the mono- or polyradicular syndromes in lumbar osteochondritis depends on the character of the disc hernia (lateral, paramedian, median) and on the degree of the reactive inflammatory changes in the radicles, the epidural tissue and the spinal meninges. Of an importance in this connection is the duration of the disease, especially, of the radicular manifestations. A particular attention should be also paid to the duration of the disease relapse.
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PMID:[Mono- and polyradicular syndromes in lumbar osteochondrosis]. 626 50

Herniation of the meninges through a defect of the spinal canal is a spinal meningocele, and is usually located dorsally in the lumbosacral region. Meningoceles are usually part of a complex developmental disorder, or of a systemic disease, or it can be iatrogenic, as well. We report a very rare case of a true anterior thoracic meningocele.
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PMID:[Thoracic meningocele]. 1720 84

Neural tube defects (NTDs) are severe congenital malformations affecting 1 in every 1000 pregnancies. 'Open' NTDs result from failure of primary neurulation as seen in anencephaly, myelomeningocele (open spina bifida), and craniorachischisis. Degeneration of the persistently open neural tube in utero leads to loss of neurological function below the lesion level. 'Closed' NTDs are skin-covered disorders of spinal cord structure, ranging from asymptomatic spina bifida occulta to severe spinal cord tethering, and usually traceable to disruption of secondary neurulation. 'Herniation' NTDs are those in which meninges, with or without brain or spinal cord tissue, become exteriorized through a pathological opening in the skull or vertebral column (e.g., encephalocele and meningocele). NTDs have multifactorial etiology, with genes and environmental factors interacting to determine individual risk of malformation. While over 200 mutant genes cause open NTDs in mice, much less is known about the genetic causation of human NTDs. Recent evidence has implicated genes of the planar cell polarity signaling pathway in a proportion of cases. The embryonic development of NTDs is complex, with diverse cellular and molecular mechanisms operating at different levels of the body axis. Molecular regulatory events include the bone morphogenetic protein and Sonic hedgehog pathways which have been implicated in control of neural plate bending. Primary prevention of NTDs has been implemented clinically following the demonstration that folic acid (FA), when taken as a periconceptional supplement, can prevent many cases. Not all NTDs respond to FA, however, and adjunct therapies are required for prevention of this FA-resistant category.
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PMID:Neural tube defects--disorders of neurulation and related embryonic processes. 2400 34