This sequence of three historical illustrations, labeled Figure 1 through Figure 3, depicts the temporal and spatial progression of a visual migraine aura (fortification spectra). Each figure presents a circular visual field with a central white fixation crosshair against a black background. The images demonstrate the characteristic 'march' of the aura from a central point toward the periphery. In Figure 1, a small, luminous, yellow-gold zig-zagged arc appears near the fixation point. In Figure 2, the disturbance has expanded into a larger crescent shape with a distinct crenellated or 'fortress-wall' border, accompanied by a trailing area of relative scotoma or blurred vision. Figure 3 illustrates the advanced stage, where the jagged, iridescent arc has migrated to the superior periphery of the visual field, significantly increasing in scale. These illustrations by James Mackenzie serve as a classic clinical representation of the neurological phenomenon of cortical spreading depression as perceived by a patient, highlighting the hallmark characteristics of teichopsia: jagged morphology, peripheral expansion, and associated visual field deficit.

This historical medical illustration, titled 'Stages of Teichopsia' (1870), is a landmark clinical diagram representing the progression of a migraine aura across the visual field. The image depicts nine chronological stages (numbered 1-9) of a visual disturbance known as a scintillation scotoma or 'fortification spectrum'. The sequence begins with a small, central point of light and evolves into an expanding, crescentic arc. The figures are characterized by their jagged, crenellated edges, resembling the bastions of a fortified town, which Hubert Airy termed 'teichopsia'. These edges feature a prismatic or polychromatic effect, with alternating segments of red, green, blue, and yellow against a dark background, illustrating the 'shimmering' or 'boiling' nature of the aura. The diagram is an important record in the history of neurology and ophthalmology, providing a subjective yet scientifically detailed mapping of transient hemiopsia and the physiological manifestation of cortical spreading depression as perceived by a patient. This content is relevant for studying the clinical presentation of migraine with aura and the history of diagnostic visualization in neurology.

This diagnostic image displays resting-state functional MRI (rs-fMRI) seed-to-voxel connectivity analysis results for patients with migraine with aura (MWA). The visual is divided into two sections, A and B, each showing three orthogonal brain views (coronal, sagittal, and axial) and an accompanying bar graph. Section A illustrates increased functional connectivity between the right antero-dorsal insula (ROI 1 R) and a posterior cluster colored in red/orange. Section B illustrates increased functional connectivity between the left antero-dorsal insula (ROI 1 L) and a similar cluster colored in blue. Blue crosshairs in both sections localize the primary cluster to the cerebellar vermis (Vermis VI/VII) and the lingual gyrus. The bar graphs compare 'Effect Sizes' between Healthy Controls (HC) and Migraine with Aura (MWA) patients, indicating significantly higher connectivity in the MWA group (p-FDR < 0.001). Anatomical landmarks visible include the cerebral cortex, corpus callosum, brainstem, and cerebellar hemispheres. This image is used to demonstrate neuro-pathophysiological differences in functional brain networks associated with migraine disorders.

This pathophysiology diagram illustrates the neurobiological mechanisms of migraine with aura, focusing on Cortical Spreading Depression (CSD) and trigeminovascular activation. A sagittal view of the human brain highlights the cortex, thalamus, hypothalamus, cerebellum, and brainstem. In the posterior cortex, CSD is represented by a red-shaded area characterized by increased extracellular potassium (K+) and excitatory glutamate (Glu). The diagram traces neurochemical signaling pathways, including serotonin (5-HT) from the Dorsal Raphe Nucleus (DRN) and norepinephrine (NA) from the Locus Coeruleus (LC) projecting to the cortex. Pain processing involves the Trigeminal Nucleus Caudalis (TNC), Periaqueductal Gray (PAG), and thalamus. The 'Headache' phase is linked to meningeal stimulation and peripheral neurogenic inflammation, shown via a detailed inset of a trigeminal neuron releasing Calcitonin Gene-Related Peptide (CGRP) onto vascular receptors. Pharmacological modulation is indicated at the bottom, showing where beta-blockers and antidepressants interfere with CSD and trigeminal hypersensitivity. This visual resource is designed for advanced medical education regarding the pathogenesis of primary headache disorders.

This pathophysiology diagram illustrates the central mechanisms of migraine, overlaid on a sagittal view of the human brain. The illustration highlights the interplay between several key neuroanatomical structures and processes. A central text box indicates 'Hypothalamic activation' leading to 'premonitory symptoms', with arrows showing its influence on the 'Spinal trigeminal nucleus' in the brainstem. Cortical spreading depression, associated with 'aura', is depicted as a large arrow targeting the same spinal trigeminal nucleus. The diagram outlines the involvement of the trigeminal nerve system, showing bidirectional activity: activation of the spinal trigeminal nucleus leads to 'Neurogenic inflammation at the trigeminal ganglion and terminal' (represented by a starburst graphic), while 'Neurotransmitter' release is shown signaling back from the brainstem to the peripheral trigeminal structures. This diagram serves as an educational tool for medical students and clinicians to understand the trigeminovascular system's role in migraine pathogenesis, specifically how hypothalamic and cortical triggers converge on the brainstem and peripheral nerve terminals.

This pathophysiology diagram illustrates the neurological pathways involved in migraine pain generation within a schematic human brain. The process begins externally with 'Triggers' leading to Cortical Spreading Depression (CSD), depicted as a curved arrow over the cerebral cortex. An oval labeled 'TVS Activation' (Trigemino-Vascular System) is situated in the frontal lobe, influenced by 'Gene mutations.' A dotted signaling pathway descends from the TVS to the 'TG' (Trigeminal Ganglion) and subsequently to the 'TNC' (Trigeminal Nucleus Caudalis) located in the brainstem. The TNC receives modulatory input from 'BN' (brainstem nuclei), such as the periaqueductal gray or locus coeruleus. Finally, a dotted arrow ascends from the brainstem toward the somatosensory areas of the cortex, labeled 'PAIN,' representing the perception of a migraine attack. This diagram serves as an educational tool for understanding the trigeminovascular system's role and the transition from cortical excitation to sensory pain perception in pediatric and adult migraine pathology.

This pathophysiology diagram illustrates the progression of cortical spreading depression (CSD) across the human brain, specifically in the context of migraine pathogenesis. The illustration shows a lateral view of the cerebral cortex, with labeled regions including the frontal, parietal, temporal, and occipital lobes, as well as the cerebellum. The CSD originates as a localized starburst icon in the occipital lobe. Gray arrows depict its anterior propagation through the parieto-occipital regions, moving across the cortical surface. The progression is shown to respect certain anatomical boundaries, marked by solid and dashed lines representing the medial and lateral sulci. In the frontal lobe, the culmination of this wave is represented by a shaded gray area labeled 'Aura,' bordered by a ring of small stars. A lightning bolt icon is positioned adjacent to the aura, signifying the neurological discharge or electrical disturbances associated with visual or sensory migraine symptoms. This diagram serves as a pedagogical tool to explain how spreading oligemia and neuronal depolarization correlate with the clinical transition from migraine triggers to symptomatic aura.