The occipital lobe sits at the back of the brain, just under your skull where you might rest a hand if you were thinking hard. It is the visual cortex. Its job is to take the patterned light that hits your retinas and turn it into the experience of seeing.
The primary visual cortex (V1, also called striate cortex because it has a visible stripe of myelin on cross-section) receives input from the eyes via the lateral geniculate nucleus of the thalamus. V1 decodes basic visual features — edges, line orientations, color contrast, simple motion. From V1, processing branches into two streams: a dorsal stream ("where" — spatial location, motion, action guidance) that extends into parietal cortex, and a ventral stream ("what" — object identity, faces, scenes) that extends into temporal cortex.
Damage to V1 produces cortical blindness — the eyes work, but the cortex cannot make sense of what they see. Smaller, more localized occipital lesions produce specific visual deficits: homonymous hemianopsia if one occipital lobe is destroyed (loss of vision in one half of the visual field of both eyes), quadrantanopsia for smaller lesions affecting one quadrant, cortical scotomas for spot lesions.
Higher-order visual areas in the temporal and parietal lobes can produce striking selective deficits. Prosopagnosia — inability to recognize faces despite normal vision — follows damage to the fusiform face area in the right inferior temporal cortex. Akinetopsia — motion blindness — follows damage to area MT/V5. Patients with akinetopsia describe a world that moves in discrete jumps, as if seen through a strobe light; pouring a cup of coffee becomes hazardous because the stream of liquid does not appear to flow.
The clinical anchor I want you to remember is the migraine aura. The zigzagging lines, the scintillating scotoma, the slowly expanding area of fortification spectra — these are produced by a wave of neuronal depolarization, called cortical spreading depression, that moves slowly across the occipital cortex at a speed of about 3 millimeters per minute. The patient experiences the wave as visual phenomena because it is happening in visual cortex. The same wave, propagating across other cortical regions, contributes to the headache phase and to the sensory and motor symptoms that some migraineurs experience.
When you read about Hildegard of Bingen's twelfth-century visions of fortified cities surrounded by stars, you may be reading about migraine aura, recorded centuries before neurology had a name for it. The visual cortex, perturbed by a slow electrical wave, is producing fortifications.