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Biomedical subjects

R Mapstone

Publications and source records attributed to R Mapstone.

17 recordsLinked to original sources

One gonioscopic fallacy.

Traditional gonioscopic practice assumes that, if most of the angle is gonioscopically closed, intraocular pressure increases. Evidence is produced to show that this is fallacious, because at its inception angle closure is iridocorneal contact occurring on the corneal side of the limbus. Although the angle cannot be seen by means of a gonioscope, there is initially no iridotrabecular contact. It is only after pressure increases that iris is pushed against trabecular meshwork and the angle is truly closed.

Aged

One model of outflow damage.

The intraocular pressure, facilities of outflow, and Po/C ratios of 3 groups of eyes were compared. Group 1 consisted of 20 eyes at risk to the development of acute closed-angle glaucoma that had been treated with prophylactic pilocarpine for at least 8 years. Group 2 consisted of 20 eyes at risk that had received no treatment and had been followed up for at least 4 years. Group 3 comprised 20 eyes in which there was no evidence of glaucoma. There were highly significant differences between the 3 groups. The 60 eyes were then provoked with pilocarpine and phenylephrine; 90% of Group 1, 75% of Group 2, and none of Group 3 developed significant gonioscopic angle closure. These results suggest that asymptomatic partial angle closure was the cause of the observed changes and provide a naturally occurring model of one mechanism that can produce outflow damage without clinical symptoms.

Anterior Chamber

Mechanisms in ocular hypertension.

This paper investigates the hypothesis that intermittent partial angle closure is one of the causes of ocular hypertension. 139 eyes from 76 patients with ocular hypertension were provoked with pilocarpine and phenylephrine. Four distinct responses appeared. Firstly, in 39 eyes (from 24 patients, 32%) gonioscopic closure of part or all of the angle appeared. Secondly, in 30 eyes (from 19 patients, 25%) no angle closure occurred but there was a substantial pigment release into the aqueous. Thirdly, in 9 eyes (from 8 patients, 11%) both angle closure and pigment release occurred. Finally, in 61 eyes (from 36 patients, 59%) neither angle closure nor pigment release appeared. (Since the 2 eyes of a patient did not always behave in the same way, for example, 1 eye might develop angle closure and the other not, 1 patient may appear in 2 groups.) From the first group 1 eye from each patient was randomly chosen for iridectomy. A repeat provocative test at least 1 year later produced a significantly different result. It is considered that the evidence obtained in this study supports the hypothesis that intermittent partial angle closure is one of the causes of ocular hypertension.

Anterior Chamber

Mechanisms in open-angle glaucoma.

One hundred and nineteen eyes from 68 patients with open-angle glaucoma were provoked by means of a pilocarpine phenylephrine provocative test. In 22% the response was the same as that seen in normal eyes. In 78% the response was the same as that seen in contralateral eyes at risk to the development of closed-angle glaucoma, which do not develop a positive provocative test. The 68 patients were randomised and 34 submitted to a "dummy" provocative test. No significant change in pressure or outflow occurred. Fifty-two of the 93 eyes with an abnormal provocative test were selected for a peripheral iridectomy and reprovoked at least 6 months after operation. The results were significantly different from those obtained before operation. It was concluded that partial-angle closure could be demonstrated in some eyes with apparent open-angle glaucoma. The mechanisms involved in the production of partial-angle closure in eyes with apparent open-angle glaucoma are discussed.

Dose-Response Relationship, Drug

Outflow changes in positive provocative tests.

The outflow changes in 26 eyes were measured during the course of a positive provocative test with pilocarpine and phenylephrine. Three separate patterns of response occurred: (1) One dose of pilocarpine and phenylephrine produced an acute attack with a large reduction in outflow. (2) The first dose of pilocarpine and phenylephrine produced a fall in pressure and increase in outflow. The second dose reversed this effect and closed the angle. (3) The first dose of pilocarpine and phenylephrine increased pressure by an insignificant amount and decreased outflow. The second dose accentuated this response and produced an acute attack.

Aqueous Humor

Outflow changes in normal eyes after closed-angle glaucoma.

Twenty-four patients with spontaneous acute closed-angle glaucoma in one eye were selected for study. All 24 eyes had a peripheral iridectomy, were normotensive, and had no gonioscopically visible peripheral anterior synechiae. Of the 24 contralateral eyes 14 gave a positive response to provocative tests and had peripheral iridectomy. The remaining 10 eyes did not give positive responses to the tests and were on no treatment. The 24 pairs of eyes were provoked with pilocarpine and phenylephrine. Tonography was performed at the start of the test, 1 1/2 hours later, and at its termination. At the start of the test the 24 eyes that had had spontaneous closed-angle glaucoma showed a higher pressure and lower outflow facility than the 24 contralateral eyes. This difference disappeared as the test progressed. It is concluded that apparently normal eyes--after an acute attack--do none the less show a significant degree of damage to the outflow system. Ten pairs of eyes from 10 normal persons were provoked in a similar fashion and at no point did a significant difference appear between right and left eyes.

Acute Disease

Normal response to pilocarpine and phenylephrine.

Fifty-eight eyes from 58 patients in which there was no evidence of glaucoma were provoked with pilocarpine and phenylephrine drops. The result was a significant reduction in intraocular pressure and a significant increase in outflow facility. The 58 eyes were randomised and 19 submitted to a 'dummy' provocative test. There was no significant change in either pressure or outflow facility. The effect of the pilocarpine/phenylephrine provocative test in normal eyes is to produce a response that is the opposite of a positive provocative test in eyes at risk of developing closed-angle glaucoma.

Drug Combinations

Dilating dangerous pupils.

Altogether 85 eyes from patients at risk to the development of closed-angle glaucoma were dilated with either parasympatholytic or sympathomimetic drugs. Of 21 eyes dilated with cyclopentolate 1/2%, 9 developed angle closure and a significantly raised pressure at some stage during dilatation and subsequent miosis. Of 58 eyes dilated with tropicamide 1/2%, 19 developed angle closure and a significantly raised pressure during dilatation. Treatment with intravenous acetazolamide and pilocarpine rapidly returned pressure to normal levels. Six eyes that had previously had a positive provocative test with simultaneous pilocarpine and phenylephrine were safely dilated with phenylephrine alone. Subsequent miosis with pilocarpine produced closed-angle glaucoma in all eyes. The significance of these observations is explained and discussed, and it is suggested that high-risk eyes should never be dilated with cyclopentolate. Tropicamide is safe if elementary precautions are observed. Safest of all, however, is phenylephrine-induced mydriasis and subsequent miosis with thymoxamine drops 1/2%.

Acetazolamide

Partial angle closure.

During the course of negative provocative test for closed-angle glaucoma using pilocarpine and phenylephrine 60% of eyes develop significant reductions in outflow facility at some stage during the test. It is shown that these reductions can be explained by postulating the presence of partial-angle closure since: (1) A random sample (6) of 53 eyes showing an abnormal response subsequently had a peripheral iridectomy. On reprovoking they then behaved as normal eyes with a uniform increase in outflow. (2) Fifty-eight eyes that had a peripheral iridectomy for closed-angle glaucoma (spontaneous or induced) responded to provocative testing as do normal eyes.

Drug Combinations

Provocative tests in closed-angle glaucoma.

Altogether 119 eyes at risk of developing closed-angle glaucoma were provoked with simultaneous pilocarpine and phenylephrine; of these 74 developed closed-angle glaucoma. The remaining 45 eyes were re-provoked with tropicamide and a further nine developed closed-angle glaucoma. The 36 eyes in which all tests were negative were given no treatment and have been observed for a period of 1 to 7 years (mean 3 years). One has developed closed-angle glaucoma. A scheme for provoking eyes at risk of developing closed-angle glaucoma is described.

Adult

The syndrome of closed-angle glaucoma.

Closed-angle glaucoma is the result of two mechanisms acting either separately or in combination: 1. Pupil block creates a greater pressure in the posterior than in the anterior chamber, pushing the iris on to the cornea. 2. Increased trabecular meshwork outflow in the presence of pupil block creates a lower pressure in the anterior chamber than in the posterior, pulling the iris on to the cornea. Three main groups of eyes manifest closed-angle glaucoma: (i) Mechanism (I) is necessary and sufficient, but (2) precludes the development of angle closure. (ii) Mechanism (I) is necessary but insufficient. Mechanism (2) must also be present. (iii) Mechanism (I) is necessary and sufficient but (I) and (2) may combine to produce an acute attack.

Amides

Miotics in closed-angle glaucoma.

The use of intravenous Diamox with variable doses of Pilocarpine was investigated in the treatment of primary closed-angle glaucoma. It was concluded that one drop of Pilocarpine 3 to 4 hrs after intravenous Diamox is the only parasympathomimetic drug necessary to terminated an acute attack.

Acetazolamide

HL-A 27 and acute anterior uveitis.

51 (30 men and 21 women) of 90 consecutive patients with acute non-granulomatous anterior uveitis were HL-A 27 positive. This frequency of 55-7 per cent compares with 8-2 per cent in controls. Twenty-three patients (18 men and 5 women) had in addition evidence of systemic disease, including ankylosing spondylitis, sacroiliitis and Reiter's syndrome, sometimes associated with psoriasis. Twenty-eight of 63 patients without evidence of systemic disease were HL-A 27 positive, suggesting that the uveitis in many of these cases has a similar aetiology to those with rheumatic disease. The uveitis associated with HL-A 27 is typically unilateral, associated with mechanical ptosis, and a painful diffusely red, photophobic, and lacrimating eye, generally lasting 3 weeks or more. Protein extravasation into the aqueous is considerable, cells are usually present in the aqueous and anterior vitreous, and keratic precipitates are never mutton fat in appearance. Recurrent episodes are characteristic. The association with HL-A 27 suggests that many if not most cases of non-granulomatous anterior uveitis have a close aetiological relationship to ankylosing spondylitis and Reiter's syndrome and it is likely that infective agents, leading to an unusual immunologically mediated inflammatory response in predisposed individuals, are involved. Ten patients with granulomatous anterior uveitis were HL-A 27 negative.

Adult

HL-A27 and anterior uveitis.

HL-A types were determined in 90 successive patients with non-granulomatous uveitis. Fifty-one were HL-A27 positive (55.7%) compared to 8.2% of controls. Of 16 patients with ankylosing spondylitis, 13 were HL-A27 positive, as were two patients with a history of Reiter's syndrome. Twenty-eight patients were HL-A27 positive but had no evidence of rheumatic disease. The findings are discussed in relation to the possible pathogenesis of uveitis.

Acute Disease