Abstract
Recent insights into the clinical presentation and pathophysiology of migraine aura
have paved the way for new treatments for this common but frequently debilitating
condition. Marked efflux of cellular potassium and glutamate contributes to the cortical
spreading depression that forms the electrophysiological basis of migraine aura phenomena.
Secondary vascular perturbations also contribute to the various symptoms of a migraine
attack. Calcitonin gene-related peptide (CGRP) plays a key role in many of these steps,
and a growing class of CGRP-antagonists have emerged as a novel, efficacious preventative
therapy. It is still not fully understood why a preponderance of migraine aura symptoms
is visual, and this issue is an active area of research. In addition, the pathophysiological
changes responsible for visual snow syndrome are under investigation. Before diagnosing
a patient with migraine aura, it is important to consider the differential diagnosis
of transient visual phenomena, with attention to clinical features that may suggest
conditions such as retinal disorders, transient ischemic attack, or occipital epilepsy.
Keywords
migraine - aura - visual snow
