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Abstract: Visual aura is a common presenting symptom of migraine to both neurologists and ophthalmologists. Features such as photopsia, fortification spectra, and the slow propagation of a scintillating scotoma across the visual field are usually considered diagnostic features of the visual aura of migraine. In the vast majority of cases, the diagnosis can be made without the need for further investigations. We present 9 patients and a further 31 cases from the literature who experienced visual aura fulfilling the diagnostic criteria for migraines but caused by focal occipital pathology. Key clinical features that could help to differentiate between the visual aura of migraine and those suggestive of a structural lesion are outlined. We review current scientific theories into the pathophysiology of visual aura, drawing on clinical and basic science research, including human functional imaging studies of migraine aura and advances in the genetic characterization of familial channelopathies, in order to explain the overlap which occurs in the clinical features of visual aura associated with migraine, cortical lesions, and epilepsy. We conclude that any disease process that is able to create a state of neuronal hyperexcitability can therefore increase an individual’s susceptibility to the development of cortical spreading depression, the electrophysiological correlate of the visual aura. [Copyright &y& Elsevier]

A recent hypothesis to enter the literature suggests that glaucoma is a neurodegenerative disease. The basis for this has been the finding of central nervous system changes in glaucoma patients on histology and neuroimaging. It is known that retinal ganglion cell pathology of any cause leads to anterograde and retrograde retinal ganglion cell degeneration, as well as trans-synaptic (transneuronal) anterograde degeneration. Trans-synaptic degeneration has been demonstrated in a range of optic neuropathies including optic nerve transection, optic neuritis, and hereditary optic neuropathies. More recently, similar changes have been confirmed in glaucoma patients using the neuroimaging techniques of voxel-based morphometry and diffusion tensor imaging. Some studies have reported brain changes in glaucoma outside the retino-geniculo-cortical pathway; however, these are preliminary and exploratory in nature. Further research is required to identify whether the degenerative brain changes in glaucoma are entirely secondary to the optic neuropathy or whether there is additional primary central nervous system pathology. This has critical implications for neuroprotective and regenerative treatment strategies and our basic understanding of glaucoma. [ABSTRACT FROM AUTHOR]

A 30-year-old woman presented with intermittent photopsia, a temporal visual field defect below the horizontal in her left eye, and flu-like symptoms. Slit-lamp and fundus examinations were unremarkable. Humphrey 30-2 threshold perimetry and 120-point screening visual field demonstrated blind spot enlargement of the left eye and a normal field in the right eye. Fundus autofluorescence, optical coherence tomography of the macula, full-field electroretinogram, electrooculogram, and multifocal electroretinogram were normal. Swept-source optical coherence tomography scan of the left optic nerve showed an intact outer retina, a remarkably thinned nerve fiber layer nasally, and peripapillary vitreous traction. Goldmann kinetic perimetry revealed a sector-shaped dense defect breaking out from the blind spot to the temporal periphery just below the horizontal in the left eye. The patient had nasal hypoplasia of the optic nerve and peripapillary vitreous traction. [ABSTRACT FROM AUTHOR]

Embolic disease of the anterior or posterior vascular territories may lead to disturbance of vision. Although death from this is uncommon, morbidity remains relatively high: Visual field loss may impair or preclude reading and driving and these are important influences on quality of life. Visual symptoms of stroke mean that patients may present to ophthalmologists with isolated visual symptoms, rather than directly to an emergency department. It is important to diagnose stroke and transient ischemic attacks accurately, as well as to manage them appropriately, as they are important harbingers of further cerebrovascular events. Ophthalmologists are therefore well placed to ensure that these patients receive appropriate acute treatment and secondary prevention. This article reviews the evidence for managing patients presenting with visual symptoms of vascular events. It reviews management of ischemic stroke in general, and compares this with management of events involving the anterior circulation by way of transient monocular visual loss or retinal artery occlusion, and posterior circulation by way of transient binocular visual loss or infarction of the visual cortex. [ABSTRACT FROM AUTHOR]

Abstract: Transient monocular blindness and amaurosis fugax are umbrella terms describing a range of patterns of transient monocular visual field loss (TMVL). The incidence rises from ≈1.5/100,000 in the third decade of life to ≈32/100,000 in the seventh decade of life. We review the vascular supply of the retina that provides an anatomical basis for the types of TMVL and discuss the importance of collaterals between the external and internal carotid artery territories and related blood flow phenomena. Next, we address the semiology of TMVL, focusing on onset, pattern, trigger factors, duration, recovery, frequency-associated features such as headaches, and on tests that help with the important differential between embolic and non-embolic etiologies [Copyright &y& Elsevier]