[Clinical aspects of the abnormal pupillary response; shedding light on pupillary response]. / De pupil belicht.

Testing the pupillary response is a quick and valuable diagnostic measure for certain neurological and ophthalmological diseases in patients. The pupillary response can aid in localizing abnormalities in important parts of the visual system and brainstem, provided that the tests are executed and interpreted correctly. When an abnormal pupillary response is found, it is important to differentiate between an afferent problem (eyeball, retina, optical nerve), brain stem pathology, or an efferent problem (parasympathetic fibers of the oculomotor nerve, iris sphincter muscle). We describe the technique of the ophthalmological examination, the normal neurophysiology and the possible abnormal pupil responses in patients with intact and decreased consciousness.

Progression of Anterograde Trans-Synaptic Degeneration in the Human Retina Is Modulated by Axonal Convergence and Divergence.

In the visual pathway of patients with multiple sclerosis (MS), the inner nuclear layer (INL) of the retina is a tight barrier for retrograde trans-synaptic degeneration. In this observational, retrospective cross-sectional study, segmented macular spectral domain optical coherence tomography (OCT) volume scans were reviewed to investigate if this observation also holds true for anterograde trans-synaptic degeneration. Significant thinning was found in all retinal layers in patients with outer retinal diseases compared with the healthy controls, while there was no significant attenuation of the outer retina in patients with MS. In contrast to the tight barrier function observed with retrograde trans-synaptic degeneration, the INL appears to be more permissive for the propagation of anterograde trans-synaptic degeneration. We speculate that this may be due to the size of the area affected and be explained by convergence and divergence of axons within the retinal layers. These findings are likely relevant to future restorative stem cell treatment of the outer retinal layers, as time may matter.

The prevalence of microcystic macular changes on optical coherence tomography of the macular region in optic nerve atrophy of non-neuritis origin: a prospective study.

BACKGROUND: Microcystic macular changes, also called microcystic macular oedema, have recently been reported in patients with multiple sclerosis, particularly after optic neuritis. But it has since emerged that the finding is not specific for optic neuritis. This study was designed to prospectively investigate the prevalence of microcystic perifoveal changes in patients with optic atrophy not due to optic neuritis. METHODS: A prospective, cross-sectional study including 54 patients with a history of optic atrophy and 54 healthy control subjects. Spectral domain optical coherence tomography (SD-OCT) was used to scan the macular area and to measure the peripapillar retinal nerve fibre layer thickness. Scanning laser ophthalmoscopy (SLO) was used for imaging of the macular area. RESULTS: Microcystic macular changes were present in 11/54 patients (20.4%), 17/90 eyes with optic atrophy (18.9%) and absent in the normal eyes of patients with monocular optic atrophy and all healthy control eyes. No correlations were found with the age, duration of optic atrophy or severity of optic atrophy. Besides the known perifoveal (semi) circular abnormal reflexes on SLO imaging, we also noticed a more patchy pattern of low SLO reflections in some patients with optic atrophy. CONCLUSIONS: Microcystic macular changes are a frequent observation in patients with optic atrophy of another cause than optic neuritis. The cause of these abnormalities remains a matter of debate. It is important for clinicians to recognise these macular changes and to realise that the cause may lie remotely away from the macula.

Recurrent Optic Perineuritis after Intranasal Cocaine Abuse.

Recurrent optic perineuritis can be related to orbital inflammation. Here we present the case of a 46-year-old male patient in whom recurrent episodes of optic perineuritis were related to chronic osteolytic sinusitis following intranasal cocaine abuse. Magnetic resonance imaging (MRI) demonstrated optic perineuritis adjacent to a soft tissue mass that intruded the orbit from the nasal cavity. Computed tomography (CT) confirmed destruction of the medial orbital wall. Staphylococcus aureus was cultured and biopsy showed granulomatous tissue. Visual outcome was poor. We review the literature and discuss the diagnostic pitfalls and management implications in relation to optic (peri)neuritis originating from the nasal sinuses.

Angiotensin converting enzyme inhibiting therapy is associated with lower vitreous vascular endothelial growth factor concentrations in patients with proliferative diabetic retinopathy.

AIMS/HYPOTHESIS: Vascular endothelial growth factor (VEGF) is thought to be instrumental in the progression of diabetic retinopathy. Indications exist that the renin-angiotensin system is involved in VEGF overexpression. We assessed the vitreous VEGF concentrations in patients and related them to anti-hypertensive treatment, with special interest in the use of ACE-inhibitors. METHODS: Samples of vitreous fluid (10-80 microl) were obtained from 39 patients both with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus and 11 non-diabetic patients undergoing intra-ocular surgery. The VEGF-A concentrations were assessed by immunoassay. RESULTS: Control patients and patients without proliferative diabetic retinopathy ( n = 8) had low and comparable VEGF concentrations (medians < 50 pg/ml). In contrast, patients with proliferative diabetic retinopathy ( n = 31) had high vitreous VEGF concentrations (median 1134 pg/ml), which showed a negative correlation with the use of ACE inhibiting medication (Spearman rank-R = - 0.54; p = 0.002, n = 13). Diastolic and systolic blood pressure did not differ significantly between the two subgroups with proliferative diabetic retinopathy, i. e. those patients receiving ACE-inhibition (medians 88/160 mm Hg, respectively) and the others (90/160). For the mostly used ACE-inhibitor in the proliferative diabetic retinopathy group, i. e. enalapril ( n = 8), a linear dose-effect relation was observed (-20 +/- 4 pg x ml(-1) x mg(-1) x day(-1); p = 0.024; coefficient +/- SEM). CONCLUSION/INTERPRETATION: Treatment with ACE-inhibitors attenuates retinal overexpression of VEGF-A in patients with proliferative diabetic retinopathy, probably by interference with a local effect of angiotensin II.