Transient visual field impairment after cold provocation in glaucoma patients with Flammer syndrome.

BACKGROUND: It is still debatable whether visual field defects in glaucoma have a reversible component and to what extent a temporary loss can be provoked. OBJECTIVE: To investigate the response of the visual function to a cold provocation in glaucoma patients, particularly to test whether subjects with Flammer syndrome (FS) behaved differently from subjects without FS. METHODS: Ten (10) primary open-angle glaucoma (POAG) patients with FS, 7 POAG patients without FS, and 11 healthy controls were tested with program G2 on the Octopus 101 perimeter before and after putting one hand in cold water (4°C) for 2 min. The mean sensitivity (MS) of each visual field was included in the statistical analysis. RESULTS: In glaucoma patients with FS, the mean MS significantly decreased after cold provocation (delta MS = -0.91 dB, CI = -1.43 to -0.39, p = 0.0014). In contrast, the mean MS in glaucoma patients without FS did not change significantly (delta MS = 0.17 dB, CI = -0.43 to 0.78, p = 0.56). Likewise, the mean MS did not change significantly in the healthy controls (delta MS = 0.23 dB, CI = -0.27 to 0.72, p = 0.36). CONCLUSIONS: Cold provocation induced a transient visual field deterioration in the glaucoma patients with FS but not in the glaucoma patients without FS or in the healthy controls. We assume this effect to be the result of a transient reduction of ocular blood flow.

Peripapillary retinal nerve fiber layer thickness measured by optical coherence tomography in different clinical subtypes of multiple sclerosis.

BACKGROUND: Multiple sclerosis (MS) is a chronic inflammatory demyelinating autoimmune disease of the central nervous system (CNS) with axonal degeneration as major determinant of neurological disability. Assessment of unmyelinated retinal nerve fibers using optical coherence tomography (OCT) may be useful for diagnosing the onset and rate of progression of neurodegeneration. OBJECTIVE: To assess the incidence and severity of damage of the peripapillary retinal nerve fiber layer (RNFL) in two different MS subtypes: non-progressive [Prog(-)MS] and progressive [Prog(+)MS]. METHODS: 48 patients (96 eyes) with MS were included: 13 males, 35 females; aged 22-62 years (mean 38.8; SD ±â€¯10.02) in two subgroups: 26 Prog(-)MS and 22 Prog(+)MS. 3 subtypes of Prog(+)MS were identified by neurologist, according to Lublin criteria: 3 patients had PPMS (14%), 7 had SPMS(32%), 12 had PRMS(54%). RRMS subtype was considered a non-progressive phenotype, designated as Prog(-)MS. All 22 patients with progressive MS phenotypes were included in one group, designated as Prog(+)MS. Progressive disease can be defined over 1 year. The expanded EDSS score was determined by the treating MS specialist and confirmed by the study investigators through the records review. Definition included a 3-strata progression magnitude in the absence of a relapse, confirmed after 3 months within the leading Functional System and required an Expanded Disability Status Scale step≥4 and pyramidal score≥2. 11 Prog(-)MS (16 eyes) and 10 Prog(+)MS (13 eyes) patients had a history of optic neuritis (ON). EDSS score was 1.5-6.5 (mean 3.83 ±â€¯1.62) in the Prog(+)MS group and 1.0-3.5 (mean 1.40 ±â€¯0.57) in the Prog(-)MS. CONTROL GROUP: 31 healthy volunteers (3 males, 28 females), aged 20-62 years (mean 37.4 ±â€¯10.88). Peripapillary RNFL thickness was measured around the optic nerve head (ONH) using spectral-domain OCT (Topcon OCT 1000 MarkII, FastMap v. 3.40, Topcon, Japan). Scans were obtained according to OSCAR-IB consensus criteria. The generalized estimating equation model (GEE) was used in the statistical analysis to assess differences in RNFL thickness between Prog(-)MS and Prog(+)MS patients, taking into consideration history of ON, EDSS score, immunomodulatory therapy, MS progression, MS duration, age and gender. The protocol was approved by the Ethical Committee of the Medical Centre of Postgraduate Education, Warsaw, Poland and informed consent was obtained from all subjects. RESULTS: There was a significant difference between Prog(-)MS and Prog(+)MS groups for mean, nasal and superior quadrant of RNFL thickness. For individuals with a history of ON, significant differences were found between the two MS phenotypes regardless of RNFL thickness measurements. CONCLUSIONS: A significant correlation was established between RNFL thickness and progression of neurodegeneration in MS patients with no regard to history of ON. RNFL thickness may be considered a MS biomarker and potential diagnostic tool for assessment of disease progression.

Choroidal infarction in a glaucoma patient with Flammer syndrome: a case report with a long term follow-up.

BACKGROUND: We present a long term follow-up of a young female patient with choroidal infarction, primary open angle glaucoma and Flammer syndrome. The patient had no classical risk factors for vascular occlusions, except for the presence of Flammer syndrome. The essential feature of this syndrome is primary vascular dysregulation, sometimes including vasospasm. The vessels of affected people respond more intensely to a number of stimuli, such as coldness or emotional stress. Any organ can be involved, including parts of the eye. The dense autonomic innervation of the choroidal vessels predisposes them particularly to vasospasms. CASE PRESENTATION: The patient was originally referred to our centre because of a deep unilateral paracentral scotoma with the presumptive diagnosis of a normal tension glaucoma. The discrepancy between the visual field defect and the optic nerve head morphology, however, led us to a vascular evaluation by a simultaneous fluorescein/indocyanine green angiography. This revealed an antecedent choroidal infarction that explained the visual field scotoma and the retinal nerve fibre layer defect in the corresponding area. During the follow-up period of 11 years, the patient also developed bilateral glaucomatous optic neuropathy despite a well-controlled intraocular pressure. CONCLUSIONS: We hypothesise that in the patient presented here, the Flammer syndrome contributed to both the acute unilateral choroidal infarction and to the chronic development of bilateral glaucomatous optic neuropathy.

Combined treatment in punctate inner choroidopathy.

PURPOSE: The purpose of this study was to describe a combination treatment for choroidal neovascular (CNV) membrane, secondary to punctate inner choroidopathy (PIC). PATIENT AND METHODS: A 44-year-old female patient was diagnosed with PIC complicated by the development of recurrent juxtafoveal neovascular membrane. The treatment included a sequence of monotherapy regimens: systemic steroid therapy, photodynamic therapy, and intravitreal injections of vascular endothelial growth factor (VEGF) inhibitor (anti-VEGF). Owing to the CNV membrane resistance to various types of monotherapy, a combination treatment consisting of local injections of steroid underneath the Tenon's capsule and intravitreal anti-VEGF injections was used. RESULTS: Systemic steroid therapy resulted in rapid local improvement with a very short remission period. No positive effects of photodynamic therapy were observed. Sequential anti-VEGF injections led to remission periods of several months. Permanent regression of CNV membrane was achieved following combined local application of steroid and intravitreal anti-VEGF injections. CONCLUSION: A combination treatment including steroid and anti-VEGF medication characterized by anti-inflammatory and antiangiogenic effects may be a very beneficial option for the treatment of recurrent CNV membrane as a complication of PIC.

Decreased endothelin-1 plasma levels in multiple sclerosis patients: a possible factor of vascular dysregulation?

BACKGROUND: Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system with possible involvement of vascular dysregulation secondary to endothelial dysfunction caused by destruction of the vessel wall. Vascular dysregulation leads to excessive vasoconstriction or insufficient vasodilatation, resulting in vasospasm mediated by endothelin-1 (ET-1), the most potent and long-lasting mediator. Vascular dysregulation can play an important role in the pathogenesis of some eye disorders and it has been hypothesized that it is a vascular risk factor for glaucomatous optic neuropathy. The aim of this study was to estimate endothelin-1 (ET-1) plasma levels in patients with MS. MATERIAL AND METHODS: The MS group consisted of 39 patients (9 males, 30 females), mean age: 38.8 ± 10.02 years, range: 22-62. The control group consisted of 27 healthy volunteers (3 males and 24 females), mean age: 37.4 ± 10.88 years, range: 20-62; clinically, in a non-active stage of the disease. ET-1 plasma levels were measured using the Endothelin-1 ELISA Kit (Immuno-Biological Laboratories Co., Japan). Statistical analysis was performed with the nonparametric Mann-Whitney U test for independent groups. RESULTS: Endothelin-1 (ET-1) plasma levels were significantly lower in MS patients compared to healthy controls: mean value 0.55 ± 0.44 pg/ml (146.05 ± 118.27 fmol/ml) vs. 0.95 ± 0.48 pg/ml (252.83 ± 127.16 fmol/ml); P=0.012. CONCLUSIONS: Significantly decreased ET-1 plasma levels in the MS patients could reflect the non-active disease at the time of ET-1 measurements or the effects of immunomodulatory treatment, but it cannot be excluded that decreased ET-1 plasma levels in these patients might result from vascular dysregulation.

Levels of antibodies against human heat shock protein (HSP) 60 in patients with glaucoma in Poland.

BACKGROUND: Although elevated intraocular pressure is a major risk factor for the development of glaucoma, there is increasing evidence that the immune system may be involved in the development of normal-tension glaucoma (NTG). The aim of this study was to determine if NTG is associated with elevated levels of antibodies against human heat shock protein (HSP) 60. MATERIAL AND METHODS: The study was conducted in 139 subjects (35 subjects with NTG [Group 1], 34 subjects with primary open-angle glaucoma /POAG/ [Group 2], 24 subjects with autoimmune rheumatic diseases [Group 3], and 36 healthy controls [Group 4]). All subjects had complete ophthalmologic examination (visual acuity, slit-lamp examination, tonometry, gonioscopy; visual-field examination, and optical coherence tomography /OCT/ of the optic nerve head and the macula). Blood samples were collected for the measurements of serum levels of antibodies against human HSP60. RESULTS: The subjects with rheumatic diseases had the highest median serum level of antibodies against HSP60 - 20.49 ng/mL. The values in the subjects with NTG, POAG, and in controls were 18.79 ng/mL, 18.61 ng/mL and 17.61 ng/mL, respectively (p=0.96). CONCLUSIONS: This study does not confirm the hypothesis that normal-tension glaucoma is associated with elevated blood levels of antibodies against human heat shock protein (HSP) 60.

[Atypical case of acute retinal necrosis secondary to the primary herpes simplex infection]. / Nietypowy przypadek ostrej martwicy siatkówki w przebiegu pierwotnego zakazenia wirusem herpes simplex.

Acute retinal necrosis is a rare manifestation of viral chorioretinitis, accompanied by occlusive vasculitis, which is associated with poor visual prognosis. The main causal factors include varicella-zoster virus in older patients and herpes simplex in younger ones. The disease typically manifests as a reactivation of latent infections. We present a case of a 57-year-old female with atypical clinical manifestation of acute retinal necrosis secondary to the primary viral infection with herpes simplex. The serology panel of vitreous tap and blood sample confirmed viral aetiology (H. simplex). The initial clinical signs included optic disc edema with retinitis presenting as self-limiting, slowly progressing, peripheral lesions, later followed by uveitis. The antiviral therapy resolved the symptoms of uveitis and enabled healing of retinal lesions, however the natural course of disease was later complicated with retinal detachment. It was successfully treated with vitreoretinal surgery. Despite aggressive treatment, the final visual outcome was unfavourable, due to optic nerve atrophy.

Selected autoantibodies and normal-tension glaucoma.

BACKGROUND: Although intraocular pressure is an important risk factor in glaucoma, there is growing body evidence indicating an immunological component in the pathogenesis of normal-tension glaucoma (NTG). The aim of this study was to determine if NTG coexists with elevated levels of autoantibodies detected in rheumatic diseases. MATERIAL AND METHODS: We enrolled 105 patients into the study: 35 with NTG, 34 with primary open-angle glaucoma (POAG), and 36 controls. All patients underwent ophthalmic examination and blood tests. Blood was examined for the level of: antibodies against antinuclear antibodies (ANA), antibodies to extractable nuclear antigens (ENA), immunoglobulins (IgG, IgA, IgM), rheumatoid factor, anti-citrullinated protein antibodies (ACPA), and antiphospholipid antibodies (anticardiolipin antibodies, beta2-glycoprotein I antibodies, antiprothrombin antibodies). RESULTS: The level of ANA was increased among 6 patients in the NTG group (17.1%), 8 in the POAG group (23.5%), and 6 in the control group (16.5%). The difference was not statistically significant (p=0.97). None of the patients in the NTG, POAG, or control group had positive antibodies to ENA. The level of immunoglobulins IgG, IgM, and IgA in the 3 groups was similar and within normal values. The median level of rheumatoid factor and ACPA was the highest in the NTG group, but it was within normal laboratory values. There was a statistically significant difference between antiprothrombin antibodies IgG between the NTG and POAG group (p=0.01), but not between the NTG and control group (p=0.24). CONCLUSIONS: The results of our study do not confirm the hypothesis that NTG coexists with elevated blood levels of antibodies, which are a characteristic feature of rheumatic diseases.

Ocular ischemic syndrome - a systematic review.

Ocular ischemic syndrome is a rare condition, which is caused by ocular hypoperfusion due to stenosis or occlusion of the common or internal carotid arteries. Atherosclerosis is the major cause of changes in the carotid arteries. Ocular ischemic syndrome is manifested as visual loss, orbital pain and, frequently, changes of the visual field, and various anterior and posterior segment signs. Anterior segment signs include iris neovascularization and secondary neovascular glaucoma, iridocyclitis, asymmetric cataract, iris atrophy and sluggish reaction to light. Posterior eye segment changes are the most characteristic, such as narrowed retinal arteries, perifoveal telangiectasias, dilated retinal veins, mid-peripheral retinal hemorrhages, microaneurysms, neovascularization at the optic disk and in the retina, a cherry-red spot, cotton-wool spots, vitreous hemorrhage and normal-tension glaucoma. Differential diagnosis of ocular ischemic syndrome includes diabetic retinopathy and moderate central retinal vein occlusion. Carotid artery imaging and fundus fluorescein angiography help to establish the diagnosis of ocular ischemic syndrome. The treatment can be local, for example, ocular (conservative, laser and surgical) or systemic (conservative and surgical treatment of the carotid artery). Since the condition does not affect the eyes alone, patients with ocular ischemic syndrome should be referred for consultation to the neurologist, vascular surgeon and cardiologist.

Comparative study of the retinal nerve fibre layer thickness performed with optical coherence tomography and GDx scanning laser polarimetry in patients with primary open-angle glaucoma.

BACKGROUND: We compared the parameters of retinal nerve fibre layer in patients with advanced glaucoma with the use of different OCT (Optical Coherence Tomograph) devices in relation to analogical measurements performed with GDx VCC (Nerve Fiber Analyzer with Variable Corneal Compensation) scanning laser polarimetry. MATERIAL/METHODS: Study subjects had advanced primary open-angle glaucoma, previously treated conservatively, diagnosed and confirmed by additional examinations (visual field, ophthalmoscopy of optic nerve, gonioscopy), A total of 10 patients were enrolled (9 women and 1 man), aged 18-70 years of age. Nineteen eyes with advanced glaucomatous neuropathy were examined. 1) Performing a threshold perimetry Octopus, G2 strategy and ophthalmoscopy of optic nerve to confirm the presence of advanced primary open-angle glaucoma; 2) performing a GDx VCC scanning laser polarimetry of retinal nerve fibre layer; 3) measuring the retinal nerve fibre layer thickness with 3 different optical coherence tomographs. RESULTS: The parameters of the retinal nerve fibre layer thickness are highly correlated between the GDx and OCT Stratus and 3D OCT-1000 devices in mean retinal nerve fibre layer thickness, retinal nerve fibre layer thickness in the upper sector, and correlation of NFI (GDx) with mean retinal nerve fibre layer thickness in OCT examinations. Absolute values of the retinal nerve fibre layer thickness (measured in µm) differ significantly between GDx and all OCT devices. CONCLUSIONS: Examination with OCT devices is a sensitive diagnostic method of glaucoma, with good correlation with the results of GDx scanning laser polarimetry of the patients.

[Complications of intravitreal injections--own experience]. / Powiklania po iniekcjach do komory ciala szklistego--doswiadczenia wlasne.

PURPOSE: Authors present complications associated with intravitreal injection perfomed in Ophthalmic Clinic CMKP MATERIAL AND METHODS: retrospective study, between January 2006 and July 2009 we performed intravitreal injections with triamcinolone acetonide (Kenalog, 4 mg), ranibizumab (Lucentis, 0.5 mg), bevacizumab (Avastin, 1.25 mg) and pegaptanib (Macugen, 0.3 mg). We treated eyes with age-related macular degeneration, diabetic macular edema, after retinal venous occlusion, with uveitis, Irvine-Gass syndrome, idiopathic juxtafoveolar teleangiectasia and central serous retinopathy. RESULTS: 943 eyes received intravitreal injections. The most common ocular complication was subconjunctival hemorrhage which was seen in 36% cases. Temporary elevated intraocular pressure above 21 mmHg was noticed in 18 eyes (5%) after anti-VEGF agents injections and in 30 eyes (23.4%) after Kenalog injection. Anterior uveitis developed in sixteen cases (1.7%) from the Avastin (5 eyes) and Lucentis (3 eyes) group. Anterior-posterior inflammation occurred in 8 eyes (0.8%), including four eyes (0.4%) with sterile endophthalmitis (3 following bevacizumab and 1 following ranibizumab injection), one eye (0.1%) with pseudoendophthalmitis (after triamcinolone). There were three cases of suspected endophthalmitis (2 following bevacizumab and 1 following triamcinolone injection). The infectious endophthalmitis after triamcinolone injection was culture-proven and revealed Staphylococcus epidermidis. Cataract formation or progression was noted in 34 eyes totally. In Kenalog group progression of cataract was seen in 23.4% of eyes (30 cases) during 2-years of follow-up and in anti-VEGF agents group--in two cases (0.6%) and 2 cases of iatrogenic cataract. Three diabetic patients suffered systemic adverse events: one patient developed renal insufficiency, one patient developed cerebrovascular accidents and one suffered a myocardial infarction resulting in death. CONCLUSIONS: Intravitreal injections are associated with a low incidence of serious adverse events. The most common ocular complication was subconjunctival hemorrhage. There was one case of serious complication--the culture-proven infectious endophthalmitis after Kenalog injection. Cataract formation and increase of intraocular pressure were more often observed following intravitreal triamcinolone injection.

Investigation into the vasospastic mechanisms in the pathogenesis of glaucomatous neuropathy.

UNLABELLED: Spasm of blood vessels supplying the optic nerve head is considered one of possible ischaemic mechanisms of glaucomatous optic neuropathy. PURPOSE: The aim of the study was to evaluate the role of two potent and long-acting vasoconstrictors: endothelin-1 (ET-1) and neuropetide Y (NPY) in the pathogenesis of glaucoma by: 1) measurement of plasma ET-1 and NPY concentrations in primary open-angle glaucoma (POAG) patients with high intraocular pressure (HTG patients) and with normal intraocular pressure (NTG patients) at baseline and following peripheral exposure to cold (cold-pressor test), 2) assessment whether changes, if any, in the plasma concentrations of both peptides following the cold-pressor test correlate with visual field defects. MATERIAL AND METHODS: The study was conducted in three groups of subjects: 1) HTG patients, 2) NTG patients and 3) controls. All subjects were young and free from any cardiovascular disorders. ET-1 and NPY concentrations in the plasma were measured by radioimmunoassay (ET-1: Amersham International UK, NPY: Peninsula Laboratories INC). The cold-pressor test was performed by immersing the whole hand in ice-cold water (4 degrees C) for 2 minutes. Visual fields were examined using standard automated perimetry (Octopus 101, G-2 programme, normal strategy). RESULTS: In the NTG patients the mean baseline plasma ET-1 concentration was significantly lower and the mean baseline plasma NPY concentration significantly higher compared to controls. On the other hand, there were no statistically significant differences in the mean baseline peptide levels between the HTG patients and the control subjects. After the cold-pressor test the mean ET-1 concentrations considerably increased in the three groups. The highest increase was seen in the NTG group and it was statistically significant compared to the HTG group and controls. Following the cold-pressor test the mean NPY concentration was significantly decreased in the NTG group, but remained virtually unchanged in the HTG group and controls. In the NTG patients, significant increase in the mean ET-1 concentration and decrease in the mean NPY concentration seen after the cold-pressor test were accompanied by a significant decrease in the mean MS (mean retinal sensitivity) value in the second eye examined after the cold-pressor test, but no correlation was found between changes in the MS values and changes in the ET-1 and NPY concentrations. There were no significant changes in the mean MS values after cold-pressor test in the HTG patients and controls. CONCLUSIONS: Our findings suggest abnormal neuro-endothelial mechanisms of vascular tone control in NTG patients, related to the effects of ET-1 and NPY, secondary to endothelial dysfunction and to dysregulation of the autonomic nervous system. These abnormalities may involve potentiation of the vasoconstrictive effects of both ET-1 and NPY leading to the optic nerve head ischaemia and subsequent development of visual field defects in the course of normal-tension glaucoma.

[Evaluation of retinal thickness in macular region in diabetic patients with RTA analyzer]. / Grubosc siatkówki w plamce u pacjentów z cukrzyca oceniania za pomoca analizatora RTA.

PURPOSE: Aim of the study is an evaluation of the anatomic state of retina in the macular region in diabetic patients with various stages of retinopathy by using RTA analyzer, and an assessment of applicability of this method in early diagnosis of diabetic macular edema. MATERIAL AND METHODS: Forty diabetic patients (68 eyes) underwent full ophthalmologic examination and also retinal thickness analysis with RTA analyzer. In particular, foveal average thickness FAV and posterior pole average thickness PPAV were determined. The data were statistically evaluated. RESULTS: Both FAV and PPAV are strongly correlated with the eyeground state and increased with increasing the severity of retinopathy and macular edema. The patients with minimal and mild nonproliferative retinopathy without any visible macular edema showed an increased retinal thickness when compared both with diabetic patients without any retinopathy and with control patients. The thickness was however lower than that in patients with diabetic macular edema. CONCLUSIONS: The eyes with minimal and mild nonproliferative diabetic retinopathy without any visible macular edema should be examined by some independent methods, like RTA. The method can be recommended for screening the macular edema in diabetic patients.

[Application of retinal nerves fiber layer examination--GDx in patients with multiple sclerosis]. / Zastosowanie badania grubosci wlókien nerwowych siatkówki--GDx u pacjentów ze stwardnieniem rozsianym.

PURPOSE: The purpose of our study is to evaluate retinal fiber layer thickness with scanning polarymetry laser (GDx), in patients suffering from SM with or without optic nerve symptoms. Multiple sclerosis proceeds to neurodegenerative changes and commonly appears with retrobulbar optic nerve damage. Examination of retinal nerves fiber layer examination with scanning laser polarymetry (GDx) enables to perform quantitative evaluation of retinal nerves fiber layer thickness within the area around the optic nerve disc. It finds application in diagnosis and monitoring of glaucoma, however its usefulness as a tool evaluating optic nerve in multiple sclerosis, has not been proved yet. MATERIALS AND METHODS: Subjects diagnosed with multiple sclerosis (SM) were divided into 2 groups. First group was comprised of subjects, who suffered from at least one episode of retrobulbar neuritis, in at least one eye. Second group was made up of 8 subjects with no history of retrobulbar neuritis. Retinal nerves fiber layer thickness was measured with scanning polarymetry laser (GDx). RESULTS: Symptoms of retinal nerves fiber layer damage, were discovered with GDx significantly more common in first group (70% vs 18.75% accordingly). CONCLUSIONS: Moreover, we stated that evaluation with scanning polarymetry laser might be precious method in discovering retinal nerves fiber layer damage in the course of multiple sclerosis. Presence of defects in retinal nerves fiber layer in patients suffering from multiple sclerosis with no history of retrobulbar neuritis may suggest subclinical damage of optic nerve.

[Neuro-hormonal regulation of aqueous humor dynamics as the basis of glaucoma pharmacotherapy. Part I. Aqueous humor secretion]. / Neurohormonalna regulacja dynamiki cieczy wodnistej jako podstawa farmakoterapii jaskry. Czesc I--Produkcja cieczy wodnistej.

The aim of this article is to present current opinion on aqueous humor dynamics regulation and antiglaucoma drugs mechanisms of action. Glaucoma pharmacotherapy is based mainly on neuro-hormonal processes controlling aqueous humor dynamics. Systemic hormones as well as local hormones and autonomic nervous system mediators are involved in the processes of aqueous humor formation and drainage. Antiglaucoma medications act mainly through activation or inhibition of these systems' receptors, helping to decrease aqueous humor production or improve aqueous humor outflow. In this article (part 1) we describe three groups of antiglaucoma medications (beta-antagonists, adrenergic agonists, carbonic anhydrase inhibitors), inhibiting the aqueous humor production and mechanisms of their hypotensive effect in the eye.

[Neuro-hormonal regulation of aqueous humor dynamics as the basis of glaucoma pharmacotherapy. Part II - Aqueous humor outflow]. / Neurohormonalna regulacja dynamiki cieczy wodnistej jako podstawa farmakoterapii jaskry. Czesc II--Odplyw cieczy wodnistej.

The aim of this article is to present current opinion on aqueous humor dynamics regulation and antiglaucoma drugs mechanisms of action. Pharmacotherapy of glaucoma is based mainly on neuro-hormonal processes controlling aqueous humor dynamics. Systemic hormones as well as local hormones and autonomic nervous system mediators are involved in the processes of aqueous humor formation and drainage. Antiglaucoma medications act mainly through activation or inhibition of these systems' receptors, helping to decrease aqueous humor production or improve aqueous humor outflow. In this article (part 2) we describe two groups of antiglaucoma medications (parasympathicomimetics, prostaglandin analogues), inhibiting the aquoeus humor outflow and mechanisms of their hypotensive effect in the eye.

[Glaucoma neuropathy and neuropathy in multiple sclerosis--common elements of pathogenesis?]. / Neuropatia jaskrowa i neuropatia w przebiegu stwardnienia rozsianego--wspólne elementy patogenezy?

UNLABELLED: The optic neuropathy in multiple sclerosis and glaucoma neuropathy are very common ophthalmological diseases. Multiple sclerosis /MS/ is the chronic inflammatory central nervous system demyelinisation disease with an autoimmunological ethiology. The last investigation of multiple sclerosis indicate the molecular and cellular autoimmunisation aspects. Te role of vasoactive factors is underlines in its pathogenesis which also suggests the common elements of glaucoma and MS pathogenesis. The over expressed vasoconstrictive mechanisms in both diseases can conduct to optic nerve injury. The aim of this study is evaluation of the optic disc morphological changes in sclerosis multiplex patients /MS/ with or without neuritis optica in anamnesis in glaucoma "remodeling" aspects. MATERIAL AND METHODS: We present two patients with coexsist sclerosis multiplex and glaucoma neuropathy, which underwent retrobulbar neuritis. CONCLUSION: Coexistance of glaucoma neuropathy and multiple sclerosis neuropathy may indicate common elements of glaucoma and SM pathogenesis. The authors recommend precise morphological optic disc evaluation in multiple sclerosis patients because glaucoma neuropathy may appear.

[Are endothelin-1 and neuropeptide Y involved in the pathogenesis of glaucoma?]. / Czy endotelina-1 i neuropeptyd Y odgrywaja role w patogenezie neuropatii jaskrowej?

Vasospasm in the vessels, supporting the optic disc, is nowadays considered one of the possible etiological factors leading to development of glaucomatous neuropathy. This article describes physiological regulatory mechanisms of blood circulation in these vessels, including influence of autonomic nervous system and blood flow autoregulation; it also explains why vasospasm may disturb autoregulation. Special attention is paid to the role of vascular endothelial mediators, which are responsible for autoregulation. Observations indicating that vasospasm may be a risk factor of glaucomatous damage are also presented. The article describes data concerning vasospastic effects of two mediators: endothelin-1 (ET-1), released by vascular endothelium, and neuropeptide Y (NPY), a sympathetic nervous system neurotransmitter, on the vessels supporting the optic disc and their possible role in producing blood flow disturbances in these vessels. Investigation results indicating that endothelial dysfunction, connected with increased ET-1 plasma levels and sympathetic nervous system disorders, may be involved in the pathogenesis of normal-tension glaucoma, are presented.