Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arachidonic acid metabolites are under investigation as possible vasoactive agents involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage. Prostaglandins, as well as other vasoactive compounds, activate contractile proteins through utilization of extracellular bound Ca++ to the intracytoplasmic free fraction. Recently, calcium-antagonists, mainly Nimodipine, have been proposed for the prophylaxis and/or reversal of the ischemic damage caused by vasospasm. Nimodipine failed to reduce vasospasm incidence in a series of 30 patients admitted with diagnosis of subarachnoid hemorrhage from ruptured intracranial aneurysm. Nimodipine failed to reduce level of four arachidonate metabolites measured (prostaglandin D2, prostacyclin, thromboxane B2 and leukotriene C4) in lumbar and cisternal CSF. After subarachnoid hemorrhage there is a significant increase of CSF levels of arachidonate metabolites; in perianeurysmic cisterns level of prostaglandin D2, thromboxane B2 and leukotriene C4 are significantly higher than lumbar CSF levels. Moreover, cisternal CSF level of prostaglandin D2 and leukotriene C4 are significantly higher in patients with symptomatic vasospasm. Nimodipine did not significantly modify CFS level of arachidonate metabolites: this suggests that Nimodipine treatment, which definitely improves long-term results of patients for intracranial aneurysms, could exert its pharmacological action reducing Ca++ intake from the extracellular compartment and preventing a direct toxic effect of calcium, without a direct action against the release of vasoactive compounds.
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PMID:Effect of nimodipine on arachidonic acid metabolites after subarachnoid hemorrhage. 312 Apr 89

To detect and identify lipid peroxides in the CFS following subarachnoid hemorrhage (SAH), CSF samples were obtained sequentially from 10 patients who developed typical vasospasm and were analyzed by HPLC and gas chromatography-mass spectrometry. One of the peaks appearing on the 7th day after SAH was identified as 5-hydroxy eicosatetraenoic acid. On HPLC, an identical peak was detected in samples from other SAH patients. The results gave unequivocal evidence that peroxides of arachidonic acid are present in the CSF following SAH, and a correlation between them and the occurrence of vasospasm seemed likely. The hypothesis that lipid peroxides are involved in the genesis of vasospasm deserves further investigation.
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PMID:Identification of 5-hydroxy eicosatetraenoic acid in cerebrospinal fluid after subarachnoid hemorrhage. 661 56

An adult case of isolated fourth ventricle which developed in the early postoperative period of SAH is reported. A 72-year-old male with Hunt & Kosnik Grade 4 subarachnoid hemorrhage (SAH) underwent emergent neck-clipping of an anterior communicating artery aneurysm along with setting of external ventricular drainage (EVD) and cisternal drainage (CD). The lamina terminalis (LT) was opened. Preoperative study had showed diffuse SAH with intraventricular hemorrhage (IVH), and mild dilatation of the whole ventricular system on CT scan (Fisher Group 4). Twelve hours after surgery, both of the drainages were opened with the pressure setting of 20 cm H2O for EVD and 10 cm H2O for CD. Although his neurological state had been improving, 2 hours after the opening of the drainages he suddenly fell into respiratory arrest and coma, when 20 ml of CFS through CD was drained. On CT scan, isolated fourth ventricle was recognized. The patient died on the ninth postoperative day. In case of severe SAH with diffuse IVH, we should be careful when setting the pressure of EVD or CD with the LT opened, because of the possibility of occlusion of the fourth ventricle outlet and aqueduct, that results in fourth ventricle isolation.
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PMID:[A case of isolated fourth ventricle in the early postoperative period of subarachnoid hemorrhage]. 1072 25

The lumbar puncture (LP) is a relatively simple diagnostic test. However, significant diagnostic ambiguity can arise when trauma from the needle causes bleeding into the subarachnoid space, especially when trying to make the diagnosis of subarachnoid hemorrhage (SAH). The purpose of this article is to assist emergency physicians in distinguishing traumatic LPs from SAH. To correctly interpret the findings of a traumatic tap, a few concepts must be understood. Timing of the LP in relation to the onset of the SAH affects the results of the cerebrospinal fluid (CFS) analysis; the typical findings will change with time. With a few caveats, xanthochromia, the yellow discoloration of the CSF resulting from hemoglobin catabolism, is often critical in making a diagnosis of SAH. A few of the most essential methods for distinguishing traumatic LP from true SAH include: the "three tube test," opening pressure, and inspection for visual xanthochromia.
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PMID:Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage. 1221 74