[Inducing factors and gonioscopic findings in 300 cases of acute glaucoma].
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We report on a case of idiopathic uveal effusion syndrome complicated by AION. To our knowledge such an association hasn't been previously described. We suggest that scleral thickening caused obstruction of vortex veins followed by uveal effusion and compression of posterior ciliary arteries within their intrascleral tract, leading to AION. Nevertheless is can't be excluded that AION was the result of mechanical compression on ciliary vessels of optic disc by choroidal detachment.
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Clonidine (0.1 mg/kg IP)-induced hypoactivity and mydriasis responses were respectively used as functional indices of pre- and postsynaptic alpha 2-adrenoceptors in mouse brain. A single injection of various antidepressant drugs had no effect on either response when measured 24 h later. However, 14 days' treatment with sibutramine HCl (3 mg/kg IP), dothiepin (50 mg/kg IP), amitriptyline (10 mg/kg IP), desipramine (10 mg/kg IP) or tranylcypromine (10 mg/kg IP) markedly attenuated both clonidine-induced hypoactivity and mydriasis. Repeated administration of zimeldine (10 mg/kg IP), mianserin (10 mg/kg IP) or clenbuterol (5 mg/kg IP) had no effect on either response. Subchronic treatment with sibutramine HCl (3 mg/kg IP; 3 days) also attenuated pre- and postsynaptic alpha 2-adrenoceptor function. Five ECS (200 V, 2 s) spread over 10 days, but not a single shock, reduced the hypoactivity and mydriasis responses to clonidine. Together, the results indicate that pre- and postsynaptic alpha 2-adrenoceptor function is attenuated by repeated treatment with those antidepressants which acutely increase synaptic levels of noradrenaline. These adrenergic receptor populations are also desensitized by ECS, although this effect is probably mediated via a different mechanism. Finally, the rapid down-regulation observed with sibutramine HCl is not confined to beta-adrenoceptors alone, because pre- and postsynaptic alpha 2-adrenoceptor function is also attenuated by 3 days of treatment with this novel antidepressant drug.
The functional status of presynaptic and postsynaptic alpha 2-adrenoceptors in murine brain was respectively monitored using the hypoactivity (sedation) and mydriasis (pupil dilatation) responses to clonidine (0.1 mg/kg IP). Both responses were attenuated 24 h after 3 days of injection of sibutramine hydrochloride (3 mg/kg IP). To ascertain whether this property was exclusive to sibutramine, the following antidepressant drugs were also tested for their ability to down-regulate alpha 2-adrenoceptors rapidly: amitriptyline, doxepin, nomifensine, desipramine, amoxapine, fluoxetine, zimeldine, tranylcypromine and mianserin. When given for 3 or 5 days at the low dose of 3 mg/kg IP, none of the other antidepressants reduced clonidine-induced hypoactivity or mydriasis. Furthermore, increasing the dose of amitriptyline, doxepin, nomifensine, desipramine, amoxapine and tranylcypromine to 10 mg/kg IP did not enable these antidepressants to attenuate the alpha 2-adrenoceptor-mediated responses after 3 days of treatment. An electroconvulsive shock (ECS; 200 V, 2 s) given once daily attenuated clonidine-induced mydriasis, but not hypoactivity, when administered for 3 days and both responses when administered for 5 days. In conclusion, this comparative study using antidepressant treatments with differing pharmacological modes of action demonstrated that sibutramine was the only drug which rapidly down-regulated pre- and postsynaptic alpha 2-adrenoceptors. ECS down-regulated postsynaptic alpha 2-adrenoceptors when given for 3 days, but required 5 days to desensitise both alpha 2-adrenoceptor populations.
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Cosmetics and ophthalmological topical preparations are the main causes of allergic contact eczema about the eye. In most cases, clinical signs are conjunctival injection, blepharitis, periorbital dermatitis and edema of lids, often combined with itching. Pure edematous swelling of the eyelids should not immediately be blamed on a contact allergy, but sufficiently evaluated to exclude a benign or malignant process of the eyelids, orbita, lacrimal duct and paranasal sinus. We present a patient with pure edematous swelling of the eyelids due to a contact allergy by the sympathicomimetic phenylephrine hydrochloride, an uncommon allergen.
RATIONALE: Spontaneous fluctuations in the size of the pupil in darkness are a recognized index of sleepiness, and these fluctuations can be quantitatively measured using the pupillographic sleepiness test (PST). The central noradrenergic system is believed to play a role in the maintenance of alertness, and there is evidence that alpha 2-adrenoceptor agonists (e.g. clonidine) decrease the activity of central noradrenergic neurones, whereas alpha 2-adrenoceptor antagonists (e.g. yohimbine) have the opposite effect. OBJECTIVE: To evaluate the effects of single oral doses of clonidine and yohimbine on spontaneous pupillary fluctuations in healthy volunteers. METHODS: Sixteen healthy male volunteers (18-25 years) participated in four weekly sessions, each associated with one oral drug condition (clonidine hydrochloride 0.2 mg, yohimbine hydrochloride 22 mg, clonidine hydrochloride 0.2 mg + yohimbine hydrochloride 22 mg), according to a balanced double-blind design. Pupil diameter was recorded continuously over 11 min in darkness using a dedicated monocular video pupillometer. Average pupil diameter, power of pupil diameter fluctuations (obtained by fast Fourier transformation), and the pupillary unrest index (PUI), a measure of cumulative changes in pupil size, were computed. Autonomic functions known to be sensitive to centrally acting noradrenergic drugs (blood pressure, heart rate and salivary output) were recorded. Subjective "alertness", "anxiety" and "contentedness" were rated using visual analogue scales. Measurements were carried out 2 h after drug ingestion. Data were analyzed by ANOVA followed by Dunnett's corrected t-test (criterion of significance P < 0.05). RESULTS: Clonidine decreased systolic and diastolic blood pressure, salivation and subjectively rated alertness, and tended to decrease pupil diameter, and to increase the power of pupillary fluctuations and PUI. On the other hand, yohimbine increased systolic and diastolic blood pressure, salivation, pupil diameter and decreased PUI. When the two drugs were given in combination they reduced each other's effects. CONCLUSIONS: These results confirm the alerting effect of the centrally acting noradrenergic activating drug yohimbine and the opposite effect of clonidine, and the suitability of the PST to detect these effects.
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BACKGROUND: Periorbital allergic contact dermatitis is a rare disease and the main differential diagnoses are atopic and seborrhoeic dermatitis. The diagnosis is based on clinical appearance, patient history and patch testing. Current systematic overviews on contact allergens involved are lacking and with changes in medical preparations, new relevant antigens may emerge. PATIENTS AND METHODS: Based on the systematic data of the information network of dermatological clinics (IVDK), patch test reactions in 48,969 patients tested between 1996 and 2000 were evaluated. A total of 763 patients suffered from periorbital dermatitis which was suspected to be due to the use of topical medication. RESULTS: The most common epidermal sensitizations in the general population were observed against nickel and fragrances. In the periorbital dermatitis group, sensitization against local anaesthetics and antibiotics was more frequent than in the general population. CONCLUSIONS: In three patients, oxybuprocain was identified as the causative agent, which has not yet been recognized as a common allergen.
BACKGROUND: High ametropia is known as a risk factor in developing amblyopia. The aim of the study was to evaluate the efficiency of a commercially available infrared videorefractometer (PowerRefractor) in examining children, and to evaluate its effectiveness in detecting amblyogenic factors of the refraction. The influence of cycloplegia was of interest. METHODS: A total of 255 eyes (-28.25 D to +7.88 D spherical equivalent) of 128 patients (1-81 years) were examined by cycloplegic retinoscopy. All of them were measured with the PowerRefractor under cycloplegia. Fifty-four of these patients (108 eyes) were additionally measured without cycloplegia. The technique of the device is based on the eccentric photorefraction method. Both eyes can be measured simultaneously from a distance of 1 m. A video-analysis of each eye is computed in three meridians. The subject can be observed in real time on a screen, and the refraction is immediately available. RESULTS: Measurement of refraction was possible at all ages. More effort was required with young children who could not cooperate well with the procedure of conventional table-top autorefractometers. The mean sensitivity in detection of any amblyogenic ametropia was 80% with and without cycloplegia. The specificity was 61% with cycloplegia and 84% without. The rate of false-negative results in the detection of anisometropia, hyperopia and astigmatism ranged from 10% to 24%. In particular, high astigmatism and hyperopia remained undiscovered. CONCLUSIONS: The reliability of the photorefractor which was the subject of the evaluation in detecting amblyogenic ametropia was comparable to that of other devices described previously in the literature. The method is suitable for use in children, but anisometropia, high astigmatic and hyperopic ametropia remained undiscovered in several cases. Commercial interest: none.
BACKGROUND: Photorefraction can be carried out in both eyes simultaneously from a distance and is therefore suitable for examination of children. This study evaluated the accuracy of a commercially available photo-refractometer (Power Refractor, Plusoptix, Erlangen, Germany) and investigated whether the working distance relaxes the accommodation sufficiently without cycloplegia. METHODS: Photo-refractometer readings were compared to cycloplegic retinoscopy. Because of the limited working range the group of patients consisted of low and moderate ametropic eyes within a spherical power of -7.0 to +5.0 D. One hundred and ninety-two eyes from 104 patients (2-81 years) were photo-refracted under cycloplegia. A subgroup of 83 eyes from 46 patients was additionally refracted without cycloplegia. RESULTS: Under cycloplegia, the Power Refractor measured the spherical equivalent slightly below that of cycloplegic retinoscopy (too much minus). The mean difference in spherical equivalent was -0.12+/-0.91 D (SD). The mean difference of cylindrical power was -0.17+/-0.73 D. The mean weighted axis difference was 0.61+/-0.71 D which is comparable to an axis deviation of 18 degrees at a cylinder power of 1.00 D. Without cycloplegia, the mean difference of the spherical equivalent was -0.73+/-1.25 D. The mean difference of cylindrical power was -0.20+/-0.65 D. The mean weighted axis difference was 0.44+/-0.58 D which is comparable to an axis deviation of 13 degrees at a cylinder power of 1.00 D. CONCLUSIONS: Without cycloplegia, the spherical equivalent of the Power Refractor tends to be underestimated due to uncontrolled accommodation, especially in children. Cycloplegia improves the accuracy in evaluating the spherical equivalent, but decreases the accuracy of cylinder power and axis.
BACKGROUND: A study was carried out to ascertain, in ophthalmologically normal subjects, the short-term effects of dipivefrin hydrochloride 0.1% on visual performance and make comparisons with pilocarpine. METHODS: Twelve normal volunteers aged 20-26 years attended on three occasions. One eye, randomly selected, received one drop of either pilocarpine 2%, dipivefrin or saline 0.9%. High- and low-contrast LogMAR acuity at 6 m and pupil diameter (measured by infra-red pupillometry) were recorded at baseline (T0) and at intervals up to 90 min following instillation of drops. Program 30-2 of the Humphrey Visual Field Analyzer (HFA) was run at T0 and at 60 min after treatment instillation (T60). Saline was always instilled at visit 1, to allow for learning effects. On visits 2 and 3 either pilocarpine or dipivefrin was randomly instilled into the treated eye. RESULTS: Pilocarpine significantly worsened the field global indices mean deviation (P < 0.001) and pattern standard deviation (P < 0.01) compared with T0. There was no significant change with dipivefrin. A significant (P = 0.01) pupil dilation from 5.44 mm (SD 0.79) at T0 to 6.19 mm (SD 1.09) at T90 occurred with dipivefrin. Pilocarpine caused significant miosis. No significant changes in LogMAR values were found with dipivefrin. Pilocarpine significantly (P < 0.01) increased LogMAR values (i.e. reduced acuity) compared with dipivefrin. At T30 the mean increase in LogMAR was 0.76 (SD 0.30) for high and 0.83 (SD 0.11) for low contrast. By T90 recovery of acuity was virtually complete. CONCLUSIONS: In normals dipivefrin causes mydriasis but does not affect the central visual field global indices (as assessed by STATPAC), or high- and low-contrast LogMAR acuity. Pilocarpine adversely affects the visual field and both measures of acuity. Knowledge of these effects is of value in glaucoma therapy and when monitoring the progression of visual loss.
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