Fifteen cases of vitreous floaters with serious psychological reactions have been collected. By using a direct ophthalmoscope, causal vitreous opacities were detected. The opacities were photodisrupted with neodymium YAG laser, using energy levels of 5 to 7*1 mJ and total energy 71 to 742-0 mJ. Symptoms completely disappeared immediately after treatment in all 15 cases. There were no intraoperative or postoperative complications noted during a follow up period of at least 1 year. To our knowledge, the use ofneodymium YAG laser to treat vitreous floaters has not been previously described. Our initial experience indicates that the treatment is simple, safe, and effective. (BrJ Ophthalmol 1993; 77: 485-488) The perception of floaters is a common complaint of ophthalmic patients, and may be symptomatic of serious vitreoretinal disorders: it may also occur commonly in otherwise normal eyes. In the latter situation floaters result from localised vitreous opacities that are products of either vitreous degenerations or posterior vitreous detachments. Although most of them will resolve spontaneously, some become coarse. Their natural history cannot be predicted. They are harmless and need no treatment. However, there are rare patients who may react so excessively to vitrous floaters that they are psychologically incapacitated. For these patients, it is worth employing more aggressive treatment to relieve their annoyance. We found that this type of floater usually results from localised vitreous opacities which could easily be photodisrupted to make the floaters disappear. Our report describes treatment using a neodymium YAG (Nd-YAG) laser for 15 patients with excellent results. As far as laser treatment was concerned, all of the above mentioned examinations were for documentation only. However, an ocular fundus examination with direct ophthalmoscopy was mandatory. Through the maximally dilated pupil, the ophthalmoscopy was initially focused on the disc, the lens wheel was moved from a lower black number toward a higher black number, and the patient was asked to move his eye from left to right. The opacity was seen to float by. Usually, they were centrally located and were less than three in number. The number of opacities was equal to that ofthe floaters; a single opacity always induced a single floater. If the number of opacities was larger than the number of floaters, the more centrally located opacities were the ones responsible for the floaters. The causal relationship between vitreous opacities and floaters was easily determined in this way. The exact locations, sizes, and shapes of the causal opacities were sketched in a three dimensional graph with the optic disc serving as a reference point. When the treatment was being performed, this graph might serve to show the exact location of the target opacity and, more importantly, to show the distance of the opacity from the retina so as to avoid damaging it. The actual distance of vitreous opacity from retina could be
Control of blood pressure involves a complex interaction of hormonal, neurologic, and cardiovascular reflexes. Leptin interacts with other neurotransmitters to regulate sympathetic cardiovascular function. Brain natriuretic peptide (BNP) has diverse physiologic effects including vasodilatation and natriuresis and suppresses the renin-aldosterone axis as well as secretion of endothelin-1 and norepinephrine. The exact mechanisms of control are unclear. We evaluated whether these pathways are disrupted in 26 male patients with autonomic dysfunction (AN) and orthostatic hypotension (NOH) due to various etiologies (mean decrease of systolic/diastolic blood pressure (SBP/DBP) = -30 ± 7 /-13 ± 3 mm Hg with lack of an adequate tachycardic response to bedside tilt) [(mean age of males = 69 ± 2 yrs; BMI = 28.5 ± 1.8)].MethodsFasting plasma levels of leptin, BNP, and hemodynamic [(changes in blood pressure (SBP/DBP), heartrate (HR)] responses to bedside tilt were evaluated in 7 patients with NOH due to diabetes mellitus (DM) [RR expiratory: inspiratory ratio = 1.03 ± .01; QTC = 435 ± 8 mm], and 19 NOH due to other etiologies (10 = primary autonomic failure: 2 = Parkinson's disease: 5 = autoimmune: 2 = other) [RR = 1.05 ± .01; QTC = 421 ± 5 mm]. The responses were compared to 10 subjects with DM without NOH [RR = 1.10 ± 0.02; QTC = 424 ± 3 mm], and 9 aged-matched control subjects [RR = 1.14 ± 0.03; QTC = 405 ± 2 mm].ResultsLeptin levels correlated with BMI (r = .6, p<.01). Both leptin and BNP levels were higher in NOH with and without DM (13.1 ± 4.2 ng/mL;112.6 ± 40.0 pg/mL and 13.7 ± 1.9 ng/mL; 137.6 ± 38.3 pg/mL) than in DM without NOH and controls (6.8 ± 1.3 ng/mL; 62.6 ± 21.3 pg/mL and 8.6 ± 3.7 ng/mL; 74.3 ± 23.4 pg/mL) (p<.001), despite lack of differences in body composition. The higher leptin and BNP levels of NOH patients correlated with more abnormal hemodynamics (r = .9; p<.001).ConclusionOur data suggest that the neuropeptides play a role in the regulation of blood pressure in patients with autonomic neuropathy.
BackgroundControl of blood pressure involves a complex interaction of hormonal, neurologic, and cardiovascular reflexes. Leptin interacts with other neurotransmitters to regulate sympathetic cardiovascular function. Brain natriuretic peptide (BNP) has diverse physiologic effects, including vasodilatation and natriuresis, and suppresses the renin-aldosterone axis as well as secretion of endothelin-1 and norepinephrine. The exact mechanisms of control are unclear. We evaluated whether these pathways are disrupted in 26 male patients with autonomic dysfunction (AN) and orthostatic hypotension (NOH) due to various etiologies (mean decrease of systolic/diastolic blood pressure (SBP/DBP) = -30 ± 7/-13 ± 3 mm Hg with lack of an adequate tachycardic response to bedside tilt) (mean age of males = 69 ± 2 yrs).MethodsFasting plasma levels of leptin, BNP, and hemodynamic [(changes in blood pressure (SBP/DBP), heartrate (HR)] responses to bedside tilt were evaluated in 7 patients with NOH due to diabetes mellitus (DM) [RR expiratory: inspiratory ratio = 1.03 ± .01; QTC = 435 ± 8 mm; BMI = 29.5 ± 3.1 kg/m2], and 19 NOH due to other etiologies (10 = primary autonomic failure: 2 = Parkinson's disease: 5 = autoimmune: 2 = other) [RR = 1.05 ± .01; QTC = 421 ± 5 mm; BMI = 28 ± 1 kg/m2]. The responses were compared to 10 subjects with DM without NOH [RR = 1.10 ± 0.02; QTC = 424 ± 3 mm; BMI = 28.4 ± 1.8 kg/m2], and 9 aged-matched control subjects [RR = 1.14 ± 0.03; QTC = 405 ± 2 mm; BMI = 28.4 ± 1.4 kg/m2].ResultsLeptin levels correlated with BMI (r = .6, p<.01). Both leptin and BNP levels were higher in NOH (13.6 ± 1.7 ng/mL; 130.9 ± 29.6 pg/mL) than in subjects without NOH (7.8 ± 1.0 ng/mL; 69.2 ± 15.5 pg/mL) (p<.001), despite a lack of differences of body composition. The higher leptin and BNP levels of NOH patients correlated with more abnormal hemodynamics and autonomic function (r = .9; p<.001).ConclusionOur data demonstrate that neurohormonal levels are abnormal in patients with orthostatic hypotension due to autonomic neuropathy. This suggests that neuropeptides may play an important role in the maintenance of normal homeostasis.
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