We measured optical and biometric parameters of emmetropic eyes as a function of age. There were approximately 20 subjects each in age groups 18-29, 30-39, 40-49, 50-59, and 60-69 years with similar male and female numbers. One eye was tested for each subject, having spherical equivalent in the range -0.88 D to +0.75 D and

Mitral stenosis, thyroid toxemia, cardiac infarction, constrictive pericarditis, and hypertension are among the common causes of auricular fibrillation. Occasionally, however, the arrhythmia is discovered fortuitously and subsequent investigation shows that structural heart disease is absent. The condition has been described. variously as benign, idiopathic, arteriosclerotic, functional, and senile fibrillation, fibrillation of unknown origin and fibrillation without heart disease. We have proposed for it the term lone auricularfibrillation. Twenty patients were selected for an analysis of the special features that characterize lone fibrillation. Apart from taking each patient's history and recording the findings of a routine clinical examination, special tests were made when necessary to exclude heart disease of any kind. An electrocardiogram was always taken, not so much to confirm the nature of the arrhythmia as to show the absence of preponderance of either ventricle and of cardiac infarction. Once, the basal metabolic rate was estimated and a radioactive iodine test used to exclude thyroid toxemia. A phonocardiogram was recorded in most of the patients to prove the absence of murmurs and added sounds, especially the mitral snap, even though they had been inaudible. Cardioscopy was carried out in each case to ensure the absence of cardiac enlargement from any source, and particularly to show that mitral valve disease was not the cause of the fibrillation. Incidence. Although this form of arrhythmia is uncommon when compared with that found in mitral stenosis, it is not rare. We have omitted an estimate of its incidence among the other causes of fibrillation because such a figure is unlikely to be a true one since the condition, through absence of symptoms, often remains undiscovered until a medical examination brings it to light. Those who have written on auricular fibrillation without heart disease (

Although the mfERG correlated significantly with the desaturated D-15 in early ARM, suggesting it operates at a sensitive level, it failed to discriminate between the control and ARM groups. In our sample, the subjective function measures were more sensitive than the mfERG measures.

Purpose To monitor visual performance in early age-related maculopathy (ARM). Methods We measured monocular visual functionFhigh-contrast visual acuity (HC-VA), central visual fields (mean sensitivity, MS), colour vision (desaturated Panel D-15), Pelli-Robson (P-R), and coneand rod-mediated multifocal electroretinograms (mfERG) in 13 ARM subjects and 13 age-matched control subjects with normal fundi at baseline and after 1 year. All had visual acuity of 6/12 or better. The mfERG data were compared to templates derived from the control group at baseline. We analysed the mfERG results by averaging the central and peripheral fields and the superior and inferior fields (CP and SI methods) and by calculating the local responses. Results The mean rod-mediated responses were significantly delayed in the ARM group for the CP (P ¼ 0.04) and the SI methods (P ¼ 0.03) at baseline compared to the control group. This did not change significantly after 1 year, whereas the mean cone-mediated responses were within the normal range at both times. Although the local analysis revealed lower amplitudes for the cone-and rod-mediated responses at baseline this was not found after 1 year and only the local rodmediated latencies were delayed at both times (Po0.01). HC-VA, desaturated Panel D-15 and P-R were significantly worse in the ARM group (Pp0.01) at baseline but did not show further significant deterioration. Progressive fundus changes were found in only two subjects (18%).

Visual hallucinations are common in older people and are especially associated with ophthalmological and neurological disorders, including dementia and Parkinson’s disease. Uncertainties remain whether there is a single underlying mechanism for visual hallucinations or they have different disease-dependent causes. However, irrespective of mechanism, visual hallucinations are difficult to treat. The National Institute for Health Research (NIHR) funded a research programme to investigate visual hallucinations in the key and high burden areas of eye disease, dementia and Parkinson’s disease, culminating in a workshop to develop a unified framework for their clinical management. Here we summarise the evidence base, current practice and consensus guidelines that emerged from the workshop.Irrespective of clinical condition, case ascertainment strategies are required to overcome reporting stigma. Once hallucinations are identified, physical, cognitive and ophthalmological health should be reviewed, with education and self-help techniques provided. Not all hallucinations require intervention but for those that are clinically significant, current evidence supports pharmacological modification of cholinergic, GABAergic, serotonergic or dopaminergic systems, or reduction of cortical excitability. A broad treatment perspective is needed, including carer support. Despite their frequency and clinical significance, there is a paucity of randomised, placebo-controlled clinical trial evidence where the primary outcome is an improvement in visual hallucinations. Key areas for future research include the development of valid and reliable assessment tools for use in mechanistic studies and clinical trials, transdiagnostic studies of shared and distinct mechanisms and when and how to treat visual hallucinations.